Related Experiment Video
Updated: Jul 22, 2025
05:58
Mouse Electroacupuncture Fixation Device Fabrication for Electroacupuncture Pretreatment in Diabetic Cardiomyopathy Mouse Model
Published on: April 18, 2025
224
Interfering with Dusp2 alleviates high glucose-induced vascular endothelial cell dysfunction by promoting p38 MAPK
Xinmiao Jiang1, Qiong Yan1, Jiaqi He1
1Department of Cardiology, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Experimental Cell Research
|July 21, 2023
Summary
Dysregulation of Dusp2 contributes to diabetic vascular endothelial cell dysfunction. Inhibiting Dusp2 or overexpressing E2F4 promotes cell repair and improves blood flow in diabetic limb ischemia.
Area of Science:
- Vascular Biology
- Molecular Medicine
- Diabetology
Background:
- Diabetic lower extremity ischemia is linked to hyperglycemia-induced vascular endothelial cell dysfunction.
- Understanding the mechanisms behind this dysfunction is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of Dusp2 in hyperglycemia-induced vascular endothelial cell dysfunction.
- To elucidate the underlying molecular mechanisms involving E2F4 and p38 MAPK signaling.
Main Methods:
- Utilized high glucose-treated human umbilical vein endothelial cells (HUVECs) and a mouse model of diabetic hindlimb ischemia.
- Assessed Dusp2, p-p38 MAPK, and E2F4 levels via Western blot and qPCR.
- Evaluated cell proliferation, migration, angiogenesis, and blood flow recovery using functional assays and imaging.
Main Results:
- Dusp2 expression was elevated in high glucose conditions and diabetic ischemia models.
- Dusp2 knockdown enhanced endothelial cell proliferation, migration, and angiogenesis, and improved blood flow recovery.
- E2F4 overexpression suppressed Dusp2, activated p38 MAPK, and promoted endothelial cell functions.
Conclusions:
- Overexpression of E2F4 mitigates hyperglycemia-induced endothelial cell dysfunction by inhibiting Dusp2 and activating p38 MAPK.
- Targeting the E2F4-Dusp2-p38 MAPK axis offers a potential therapeutic strategy for diabetic vascular complications.
More Related Videos
08:15Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease
Published on: May 10, 2024
611
07:15Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
477
Related Concept Videos
01:19Interactions Between Signaling Pathways
6.3K
Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
6.3K
01:58Cell Specific Gene Expression
13.6K
Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
13.6K
01:25cAMP-dependent Protein Kinase Pathways
6.4K
Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
6.4K
02:23Abnormal Proliferation
4.6K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.6K
01:07MAPK Signaling Cascades
5.7K
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.7K
01:22PI3K/mTOR/AKT Signaling Pathway
3.7K
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...
3.7K