GO:1904346 positive regulation of gastric mucosal blood circulation: Vascular Control, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:1904346 describes any process that activates or increases the frequency, rate or extent of gastric mucosal blood circulation, a biological_process annotation in the Gene Ontology.
• Gastric mucosal blood flow is a local, microvessel-level phenomenon that determines oxygen delivery to the stomach lining and is disturbed in peptic ulcer disease and gastric carcinoma.
• The term is experimentally tractable using isolated rat gastric microvascular endothelial cells, which provide a validated in vitro model for gastric angiogenesis and microvascular biology.
• Several vasoactive and angiogenic proteins, including VCAM-1, EMMPRIN/CD147, maspin and atrial natriuretic peptide, have been linked to gastric mucosal vascular biology and gastric cancer progression.
• Bone marrow-derived mesenchymal progenitor cells can contribute to gastric epithelium, indicating that non-resident cell populations may influence mucosal vascular remodeling.
• CRISPR knockout, point-mutation, knock-in and overexpression models, combined with CRISPR library screening and bioinformatics, allow causal testing of candidate regulators of gastric mucosal blood circulation.
Description
GO:1904346, positive regulation of gastric mucosal blood circulation, is a Gene Ontology biological_process term defined as any process that activates or increases the frequency, rate or extent of gastric mucosal blood circulation. The gastric mucosa is a highly metabolic tissue that depends on continuous microvascular perfusion to maintain oxygenation and mucosal integrity, and local factors regulating vascular blood flow are central to the development of gastric mucosal hypoxia in peptic ulcer disease. Because the term is a positive-regulation node, it captures upstream signals and cellular effectors that enhance, rather than simply maintain, mucosal perfusion. Researchers study GO:1904346 because it sits at the intersection of vascular biology, epithelial repair and gastric disease. Disturbances in gastric mucosal blood flow are associated with ulcer formation and impaired healing, and the same microvascular programs are co-opted during tumor angiogenesis in gastric carcinoma. The term therefore provides a controlled vocabulary for annotating genes and pathways that increase mucosal blood circulation, enabling consistent comparison across studies of gastric physiology and pathology. Mechanistically, positive regulation of gastric mucosal blood circulation is mediated by vasoactive peptides, endothelial adhesion molecules and angiogenic factors acting on gastric microvessels. Atrial natriuretic peptide-immunoreactive cells lie in close spatial relationship with microvessels in the rat gastric mucosa, suggesting local paracrine control of mucosal perfusion. In parallel, molecules such as VCAM-1 and EMMPRIN/CD147 are overexpressed in gastric carcinoma and contribute to tumor angiogenesis and metastasis, linking mucosal vascular regulation to malignant progression. Isolated rat gastric microvascular endothelial cells provide a reductionist system in which these regulatory events can be dissected in vitro.
positive regulation of gastric mucosal blood circulation At A Glance
| GO ID | GO:1904346 |
|---|---|
| GO term | positive regulation of gastric mucosal blood circulation |
| Ontology | biological_process |
| Synonym | activation of gastric mucosal blood circulation; upregulation of gastric mucosal blood circulation; positive regulation of stomach mucosal blood circulation |
| Major function | Increases the frequency, rate or extent of blood flow through gastric mucosal microvessels |
| Parent process | Regulation of gastric mucosal blood circulation (positive-regulation branch) |
| Physiological context | Oxygen and nutrient delivery to the gastric epithelium; mucosal protection and repair |
| Pathological context | Gastric mucosal hypoxia in peptic ulcer disease; tumor angiogenesis in gastric carcinoma |
| Experimental model | Isolated rat gastric microvascular endothelial cells for in vitro gastric angiogenesis studies |
What Is GO:1904346?
In plain terms, GO:1904346 describes any biological process that switches on or boosts the flow of blood through the microvessels of the stomach lining. Formally, it is defined as any process that activates or increases the frequency, rate or extent of gastric mucosal blood circulation, and it is classified as a biological_process in the Gene Ontology. The term is a positive-regulation child of gastric mucosal blood circulation and is synonymous with activation, up-regulation or upregulation of gastric mucosal blood circulation and of stomach mucosal blood circulation. It excludes processes that merely maintain baseline perfusion or that decrease mucosal blood flow, and it is distinct from systemic cardiovascular regulation because its scope is restricted to the gastric mucosa.
Why Is positive regulation of gastric mucosal blood circulation Important in Cell Biology?
GO:1904346 matters because gastric mucosal blood circulation is a determinant of mucosal oxygenation and integrity, and its positive regulation is required to prevent or reverse the hypoxia that develops in peptic ulcer disease. The same microvascular programs that increase mucosal perfusion under physiological conditions are hijacked during gastric tumor angiogenesis, where molecules such as VCAM-1 and EMMPRIN/CD147 promote vessel formation, invasion and metastasis. Annotating genes to this term therefore helps researchers separate protective mucosal vascular responses from pathological angiogenic responses, and provides a framework for testing candidate regulators in gastric microvascular endothelial cell models.
• Gastric mucosal blood flow is a local factor whose dysregulation contributes to hypoxia of the gastric mucosa in peptic ulcer disease.
• Positive regulation of mucosal perfusion supports oxygen delivery to the metabolically active gastric epithelium.
• Gastric microvascular endothelial cells are a validated in vitro model for studying gastric angiogenesis and microvascular regulation.
• VCAM-1 overexpression is associated with oncogenesis, tumor angiogenesis and metastasis of gastric carcinoma, linking vascular regulation to cancer.
• EMMPRIN/CD147 upregulation contributes to growth and angiogenesis of gastric carcinoma and is a marker of local invasion and prognosis.
• Atrial natriuretic peptide-immunoreactive cells are spatially related to microvessels in rat gastric mucosa, implicating local vasoactive peptides in perfusion control.
• Maspin expression has clinicopathological significance in tumorigenesis and progression of gastric cancer, connecting protease-inhibitor biology to gastric vascular pathology.
• Bone marrow-derived mesenchymal progenitor cells can contribute to gastric epithelium, suggesting a role for non-resident progenitors in mucosal remodeling.
• Gastric estrogen signaling influences pituitary estrogen receptor alpha and prolactin mRNAs under different pathological conditions of the liver, illustrating endocrine modulation of gastric biology.
• The term provides a standardized annotation target for CRISPR-based causal studies of gastric mucosal vascular regulators.
What Happens During positive regulation of gastric mucosal blood circulation?
Initiation by local vasoactive and paracrine signals
In simple terms: The process starts when local chemical signals tell the stomach lining's small blood vessels to open up.
Positive regulation of gastric mucosal blood circulation is initiated by local factors that act on gastric microvessels. In the rat gastric mucosa, atrial natriuretic peptide-immunoreactive cells are located in close relationship with microvessels, indicating that locally released vasoactive peptides can act in a paracrine manner on mucosal vessels. Local factors regulating vascular blood flow are also implicated in the development of hypoxia of the gastric mucosa in peptic ulcer disease, showing that these initiation signals are clinically relevant.
Endothelial cell activation and microvascular remodeling
In simple terms: The cells that line the small blood vessels become activated and reorganize to increase flow capacity.
Once initiated, positive regulation of gastric mucosal blood circulation involves activation of gastric microvascular endothelial cells. Isolated rat gastric microvascular endothelial cells have been characterized as a model for studying gastric angiogenesis in vitro, providing direct evidence that these cells are the effector compartment for mucosal microvascular responses. Endothelial activation in this compartment can be driven by adhesion and matrix-associated molecules, as shown by the contribution of VCAM-1 and EMMPRIN/CD147 to gastric tumor angiogenesis.
Angiogenic amplification in gastric carcinoma
In simple terms: In stomach cancer, the same vessel-growing signals get amplified and help the tumor build its own blood supply.
In pathological settings, positive regulation of gastric mucosal blood circulation overlaps with tumor angiogenesis. VCAM-1 overexpression is associated with oncogenesis, tumor angiogenesis and metastasis of gastric carcinoma, indicating that adhesion-molecule signaling can amplify mucosal vascular responses. Similarly, upregulated EMMPRIN/CD147 contributes to growth and angiogenesis of gastric carcinoma and serves as a marker for local invasion and prognosis. Maspin expression also has clinicopathological significance in tumorigenesis and progression of gastric cancer, adding a protease-inhibitor dimension to gastric vascular pathology.
Contribution of non-resident progenitor cells
In simple terms: Cells from the bone marrow can travel to the stomach and help rebuild its lining and vessels.
Bone marrow-derived mesenchymal progenitor cells include a subset that can contribute to the gastric epithelium, demonstrating that non-resident cell populations participate in gastric mucosal renewal. Because mucosal renewal and mucosal perfusion are functionally coupled, this progenitor contribution provides a potential source of cells that influence positive regulation of gastric mucosal blood circulation during repair and remodeling.
Endocrine and systemic modulation
In simple terms: Hormones from elsewhere in the body can also change how the stomach's blood vessels behave.
Gastric mucosal vascular responses are subject to endocrine modulation. Gastric estrogen increases pituitary estrogen receptor alpha and prolactin mRNAs during different pathological conditions of the liver, showing that gastric endocrine signals can vary with systemic disease states. Such systemic inputs can intersect with local vasoactive and angiogenic pathways to shape the overall level of positive regulation of gastric mucosal blood circulation.
Key Genes Involved in GO:1904346 positive regulation of gastric mucosal blood circulation
The following genes and proteins have been experimentally linked to gastric mucosal vascular biology, gastric angiogenesis or gastric mucosal disease, and are therefore candidate regulators or readouts for studies of GO:1904346.
| Gene | Major Role | Research Relevance |
|---|---|---|
| VCAM-1 | Endothelial adhesion molecule linked to tumor angiogenesis and metastasis | Marker and candidate effector of gastric mucosal vascular responses in carcinoma |
| EMMPRIN/CD147 | Matrix-associated molecule contributing to growth and angiogenesis of gastric carcinoma | Prognostic marker for local invasion and target for angiogenesis studies |
| Maspin | Protease inhibitor with clinicopathological significance in gastric cancer progression | Candidate modifier of gastric tumorigenesis and vascular pathology |
| ANP (atrial natriuretic peptide) | Vasoactive peptide produced by cells closely related to rat gastric mucosal microvessels | Local paracrine regulator of gastric mucosal perfusion |
| Gastric microvascular endothelial cell markers | Define the endothelial compartment of gastric microvessels | In vitro model system for gastric angiogenesis and microvascular regulation |
| Bone marrow-derived mesenchymal progenitor markers | Identify a progenitor subset contributing to gastric epithelium | Source of non-resident cells influencing mucosal remodeling |
| Estrogen receptor alpha | Mediates gastric estrogen effects on pituitary gene expression | Endocrine modulator of gastric biology under systemic disease conditions |
| Prolactin | Pituitary hormone regulated by gastric estrogen signals | Systemic endocrine readout in gastric-liver pathology models |
| Local vascular blood flow regulators | Regulate vascular blood flow and mucosal hypoxia in peptic ulcer disease | Direct physiological determinants of GO:1904346 activity |
| Gastric mucosal hypoxia markers | Reflect insufficient mucosal perfusion | Readouts for loss of positive regulation of gastric mucosal blood circulation |
| Tumor angiogenesis effectors | Drive vessel formation in gastric carcinoma | Pathological amplification of mucosal vascular programs |
| Adhesion and matrix remodeling proteins | Support endothelial activation and invasion | Candidate CRISPR targets for vascular phenotype screens |
| Gastric epithelial progenitor markers | Mark bone marrow-derived cells contributing to gastric epithelium | Link mucosal renewal to vascular remodeling |
| Vasoactive peptide receptors | Transduce local peptide signals on gastric microvessels | Candidate nodes for pharmacological and genetic perturbation |
| Protease-inhibitor network components | Modulate tumorigenesis and progression in gastric cancer | Candidate modifiers of gastric vascular pathology |
How Is positive regulation of gastric mucosal blood circulation Regulated?
Positive regulation of gastric mucosal blood circulation is controlled at multiple levels. Locally, vasoactive peptides such as atrial natriuretic peptide are positioned to act on gastric mucosal microvessels in a paracrine manner, providing rapid modulation of perfusion. Endothelial adhesion and matrix-associated molecules, including VCAM-1 and EMMPRIN/CD147, can amplify microvascular responses and are overexpressed in gastric carcinoma, linking regulation of this process to tumor angiogenesis. Systemically, gastric endocrine signals such as estrogen can alter pituitary estrogen receptor alpha and prolactin mRNAs under different pathological conditions of the liver, indicating that endocrine status can indirectly shape gastric mucosal biology. Finally, local factors regulating vascular blood flow determine whether the mucosa becomes hypoxic in peptic ulcer disease, so the balance between positive and negative regulation of mucosal perfusion is clinically decisive.
positive regulation of gastric mucosal blood circulation and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| VCAM-1 | Gastric carcinoma oncogenesis, tumor angiogenesis and metastasis | Knockout and overexpression in gastric microvascular endothelial cell cultures |
| EMMPRIN/CD147 | Gastric carcinoma growth, angiogenesis and local invasion | Point-mutation and knock-in models in gastric cancer cell lines |
| Maspin | Gastric cancer tumorigenesis and progression | Knockout and overexpression in gastric epithelial cancer models |
| ANP | Local regulation of gastric mucosal microvessels | Knock-in reporter and knockout models in rodent gastric mucosa |
| Bone marrow-derived mesenchymal progenitors | Contribution to gastric epithelium and mucosal remodeling | Tagged knock-in lineage tracing in gastric regeneration models |
Peptic ulcer disease and gastric mucosal hypoxia
Local factors that regulate vascular blood flow are directly implicated in the development of hypoxia of the gastric mucosa in peptic ulcer disease. When positive regulation of gastric mucosal blood circulation fails or is insufficient, mucosal oxygenation is compromised, which can impair epithelial integrity and healing. This makes GO:1904346 a physiologically meaningful annotation for genes whose manipulation alters mucosal perfusion in ulcer models.
Gastric carcinoma and tumor angiogenesis
Gastric carcinoma co-opts mucosal vascular programs for tumor angiogenesis. VCAM-1 overexpression is associated with oncogenesis, tumor angiogenesis and metastasis of gastric carcinoma, and upregulated EMMPRIN/CD147 contributes to growth and angiogenesis of gastric carcinoma while serving as a marker of local invasion and prognosis. Maspin expression also has clinicopathological significance in tumorigenesis and progression of gastric cancer. Together these findings show that positive regulation of gastric mucosal blood circulation is mechanistically entangled with malignant progression.
Systemic and endocrine disease interactions
Gastric biology is modulated by systemic disease states. Gastric estrogen increases pituitary estrogen receptor alpha and prolactin mRNAs during different pathological conditions of the liver, demonstrating that hepatic pathology can alter gastric endocrine signaling. Because endocrine signals can influence mucosal vascular behavior, systemic disease should be considered when interpreting phenotypes related to GO:1904346.
Mucosal regeneration and progenitor contribution
A bone marrow-derived mesenchymal progenitor cell subset can contribute to the gastric epithelium, indicating that non-resident progenitors participate in mucosal regeneration. Since regeneration and perfusion are coupled, defects in progenitor recruitment could indirectly affect positive regulation of gastric mucosal blood circulation during repair.
From positive regulation of gastric mucosal blood circulation-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a candidate gene required for gastric mucosal perfusion? | CRISPR knockout in gastric microvascular endothelial cells |
| Does a specific variant alter endothelial angiogenic behavior? | CRISPR point mutation in gastric microvascular endothelial cells |
| Can a vasoactive peptide reporter track mucosal vascular signals? | Tagged knock-in of the peptide gene in rodent gastric mucosa |
| Does overexpression of an adhesion molecule increase angiogenesis? | CRISPR overexpression of VCAM-1 in gastric endothelial or carcinoma cells |
| Does a matrix-associated molecule drive invasion and angiogenesis? | CRISPR overexpression or knock-in of EMMPRIN/CD147 in gastric cancer cells |
| Which genes modify gastric mucosal vascular phenotypes at scale? | CRISPR library screening in gastric microvascular endothelial cells |
How to Study the positive regulation of gastric mucosal blood circulation Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Gastric microvascular endothelial cell culture | Endothelial phenotype and angiogenic capacity | In vitro modeling of gastric angiogenesis |
| Immunohistochemistry | Protein localization relative to microvessels | Mapping vasoactive peptide cells in gastric mucosa |
| In vitro angiogenesis assay | Tube formation and endothelial reorganization | Testing candidate regulators of mucosal vascular responses |
| Mucosal hypoxia assessment | Adequacy of mucosal perfusion | Evaluating loss of positive regulation in ulcer models |
| Expression profiling of gastric carcinoma | VCAM-1, EMMPRIN/CD147 and maspin levels | Correlating vascular markers with invasion and prognosis |
| Lineage tracing | Contribution of bone marrow-derived progenitors to gastric epithelium | Studying mucosal regeneration and remodeling |
| Endocrine gene expression assays | Estrogen receptor alpha and prolactin mRNAs | Assessing systemic modulation of gastric biology |
Isolation and culture of gastric microvascular endothelial cells
Isolation and characterization of rat gastric microvascular endothelial cells provides a primary in vitro system for studying gastric angiogenesis and microvascular regulation. These cultures allow controlled manipulation of candidate genes and direct measurement of endothelial behaviors relevant to positive regulation of gastric mucosal blood circulation.
Expression and localization analysis in gastric tissue
Immunohistochemistry and in situ approaches can localize vasoactive peptides relative to microvessels, as shown for atrial natriuretic peptide-immunoreactive cells in rat gastric mucosa. Similar methods can assess expression of VCAM-1, EMMPRIN/CD147 and maspin in gastric carcinoma specimens and correlate them with clinicopathological features.
Functional angiogenesis and perfusion assays
In vitro angiogenesis assays using gastric microvascular endothelial cells can quantify tube formation and migration as proxies for mucosal vascular responses. In vivo, assessment of mucosal hypoxia and local vascular blood flow regulation provides physiological readouts of whether positive regulation of gastric mucosal blood circulation is intact.
Lineage tracing and progenitor contribution studies
Bone marrow-derived mesenchymal progenitor cells that contribute to the gastric epithelium can be tracked using lineage-tracing strategies to determine how non-resident cells influence mucosal remodeling and, indirectly, mucosal perfusion. Such studies complement endothelial-focused assays by defining the cellular sources of vascular support.
How CRISPR Can Be Used to Study GO:1904346 positive regulation of gastric mucosal blood circulation
Knockout
CRISPR knockout of candidate genes in gastric microvascular endothelial cells can test whether a factor is required for endothelial activation and angiogenesis, the effector arm of positive regulation of gastric mucosal blood circulation. Knockout of adhesion or matrix-associated molecules such as VCAM-1 or EMMPRIN/CD147 in gastric carcinoma cells can reveal their contribution to tumor angiogenesis and invasion.
Point Mutation
CRISPR point mutation allows precise testing of residues or variants hypothesized to alter protein function in gastric vascular biology. For example, disease-associated or functional variants in EMMPRIN/CD147 or maspin can be introduced into gastric cell models to determine whether they change angiogenic or invasive phenotypes.
Knock-in
Knock-in strategies can place reporters or tags at endogenous loci to track vasoactive peptide expression and localization relative to gastric microvessels, as exemplified by atrial natriuretic peptide-immunoreactive cells in rat gastric mucosa. Tagged knock-in of progenitor markers can also trace bone marrow-derived cells contributing to gastric epithelium.
Overexpression
CRISPR-mediated overexpression of candidate genes such as VCAM-1 or EMMPRIN/CD147 in gastric endothelial or carcinoma cells can test sufficiency for angiogenesis and invasion phenotypes. Overexpression models complement knockout by establishing whether increased dosage of a factor is sufficient to enhance mucosal vascular responses.
How EDITGENE Supports positive regulation of gastric mucosal blood circulation Research
Researchers studying positive regulation of gastric mucosal blood circulation-related genes often need to determine whether a candidate gene is causally involved in endothelial activation, angiogenesis or mucosal perfusion, rather than merely correlated with disease. Establishing causality requires controlled genetic perturbation in relevant gastric cell models, followed by functional readouts such as angiogenic capacity and marker expression. EDITGENE provides the full spectrum of CRISPR cell-model engineering and screening services needed to build and interrogate such models.
Contact EDITGENE today to design your custom CRISPR model for positive regulation of gastric mucosal blood circulation research.
Frequently Asked Questions About positive regulation of gastric mucosal blood circulation
What is GO:1904346 positive regulation of gastric mucosal blood circulation?
GO:1904346 is a Gene Ontology biological_process term defined as any process that activates or increases the frequency, rate or extent of gastric mucosal blood circulation.
What does positive regulation of gastric mucosal blood circulation mean in simple terms?
It means any biological signal or mechanism that boosts blood flow through the small vessels of the stomach lining, helping to keep the mucosa oxygenated.
Why is gastric mucosal blood circulation important in peptic ulcer disease?
Local factors regulating vascular blood flow determine whether the gastric mucosa becomes hypoxic, and such hypoxia is implicated in peptic ulcer disease.
What genes are involved in gastric mucosal vascular biology?
Genes and proteins linked to gastric mucosal vascular biology include VCAM-1, EMMPRIN/CD147, maspin and atrial natriuretic peptide, based on studies in gastric carcinoma and rat gastric mucosa.
How do researchers model gastric angiogenesis in vitro?
Isolated rat gastric microvascular endothelial cells have been characterized as a model for studying gastric angiogenesis in vitro.
Is positive regulation of gastric mucosal blood circulation linked to cancer?
Yes, mucosal vascular programs overlap with tumor angiogenesis; VCAM-1 overexpression and EMMPRIN/CD147 upregulation are associated with angiogenesis and metastasis in gastric carcinoma.
What role do bone marrow-derived cells play in the gastric mucosa?
A bone marrow-derived mesenchymal progenitor cell subset can contribute to the gastric epithelium, indicating a role in mucosal renewal and remodeling.
How can CRISPR be used to study GO:1904346?
CRISPR knockout, point mutation, knock-in and overexpression in gastric microvascular endothelial or carcinoma cells allow causal testing of candidate regulators of mucosal vascular responses.
What methods measure gastric mucosal perfusion and hypoxia?
Assessment of local vascular blood flow regulation and mucosal hypoxia provides physiological readouts of whether positive regulation of gastric mucosal blood circulation is intact.
Does endocrine signaling affect gastric mucosal biology?
Gastric estrogen increases pituitary estrogen receptor alpha and prolactin mRNAs under different pathological conditions of the liver, showing that endocrine signals can modulate gastric biology.
Conclusion
GO:1904346, positive regulation of gastric mucosal blood circulation, provides a precise Gene Ontology framework for annotating processes that increase blood flow through gastric mucosal microvessels. Its physiological importance is underscored by the role of local vascular regulators in gastric mucosal hypoxia during peptic ulcer disease, and its pathological relevance is evident in the angiogenic programs of gastric carcinoma involving VCAM-1 and EMMPRIN/CD147. Because the process is experimentally accessible through gastric microvascular endothelial cell models and measurable through angiogenesis, expression and hypoxia readouts, it is well suited to CRISPR-based causal studies. Combining knockout, point-mutation, knock-in and overexpression models with library screening and bioinformatics enables systematic identification of the genes that positively regulate gastric mucosal blood circulation.
References
- 1. Ding YB et al.. 2003. Association of VCAM-1 overexpression with oncogenesis, tumor angiogenesis and metastasis of gastric carcinoma.. World J Gastroenterol 9(7):1409-14 PMID: 12854131
- 2. Jones MK et al.. 2000. Isolation and characterization of rat gastric microvascular endothelial cells as a model for studying gastric angiogenesis in vitro.. J Physiol Pharmacol 51(4 Pt 2):813-20 PMID: 11220490
- 3. Pasechnikov VD et al.. 1988. [The role of local factors regulating vascular blood flow in the development of hypoxia of the gastric mucosa in peptic ulcer].. Ter Arkh 60(12):74-7 PMID: 3247660
- 4. Kobayashi H et al.. 2013. Gastric estrogen increases pituitary estrogen receptor α and prolactin mRNAs during the different pathological conditions of the liver.. Endocrine 43(1):170-83 PMID: 22843122
- 5. Zheng HC et al.. 2006. Upregulated EMMPRIN/CD147 might contribute to growth and angiogenesis of gastric carcinoma: a good marker for local invasion and prognosis.. Br J Cancer 95(10):1371-8 PMID: 17088917
- 6. Okumura T et al.. 2009. Identification of a bone marrow-derived mesenchymal progenitor cell subset that can contribute to the gastric epithelium.. Lab Invest 89(12):1410-22 PMID: 19841619
- 7. Li CH et al.. 2006. Relationship between atrial natriuretic peptide-immunoreactive cells and microvessels in rat gastric mucosa.. Acta Pharmacol Sin 27(2):205-11 PMID: 16412270
- 8. Wang MC et al.. 2004. Maspin expression and its clinicopathological significance in tumorigenesis and progression of gastric cancer.. World J Gastroenterol 10(5):634-7 PMID: 14991928
