Background: The expression of gax, an anti-proliferative homeobox gene, is rapidly down-regulated in vascular smooth muscle cells (VSMCs) following arterial injury. Whether the down-regulation of gax is involved in modulating the proliferation of smooth muscle cells of the splenic vein in patients with portal hypertension has not yet been elucidated. The aim of this study was to investigate the expression of the mRNA of the gax gene in smooth muscle cells of the splenic vein in patients with portal hypertension.

Methods: Reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the expression of gax mRNA and immunohistochemistry staining was performed to demonstrate the expression of PCNA protein in the splenic veins of 28 patients with portal hypertension and those of 12 normal controls. This study was approved by the Institutional Ethics Committee and informed consent was obtained from all participants.

Results: RT-PCR showed that the expression of gax mRNA was PCNA-positive and negative in the splenic vein of patients with portal hypertension (1.08+/-0.04 and 1.39+/-0.27, respectively). There was a significant difference in the 28 patients compared with the 12 normal controls (P<0.01). The relative expression of PCNA protein in the vascular tissues was significantly higher in the experimental group than in the control group.

Conclusions: Down-regulation of gax mRNA and the overexpression of PCNA protein were seen in smooth muscle cells of the splenic vein in patients with portal hypertension, regulating the proliferation, migration and phenotypic change and resulting in remodelling of the splenic vein, which may play an important role in the pathogenesis and maintenance of portal hypertension.

Download full-text PDF

Source

Publication Analysis

Top Keywords

smooth muscle
16
muscle cells
16
splenic vein
16
portal hypertension
16
patients portal
16
cells splenic
12
expression gax
12
vein patients
12
down-regulation gax
8
gax gene
8

Similar Publications

In the mammalian ureters, the lamina propria presents as a prominent layer of connective tissue underneath the urothelium. Despite its important structural and signaling functions, little is known how the lamina propria develops. Here, we show that in the murine ureter, the lamina propria arises at late fetal stages and massively increases by fibrocyte proliferation and collagen deposition after birth.

View Article and Find Full Text PDF

Introduction: T helper 17 (Th17) cells have a significant effect in the pathogenesis of asthma, and signal transducer and activator of transcription 3 (STAT3) pathway activation is critical for Th17 cell differentiation. Timosaponin A-III (TA3) was reported to inhibit the STAT3 pathway. Here, we investigated whether TA3 improved asthma by inhibiting the STAT3 pathway.

View Article and Find Full Text PDF

Inhibition of aortic CX3CR1+ macrophages mitigates thoracic aortic aneurysm progression in Marfan syndrome in mice.

J Clin Invest

January 2025

Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China.

The pathogenesis of thoracic aortic aneurysm (TAA) in Marfan syndrome (MFS) is generally attributed to vascular smooth muscle cell (VSMC) pathologies. However, the role of immune cell-mediated inflammation remains elusive. Single-cell RNA sequencing identified a subset of CX3CR1+ macrophages mainly located in the intima in the aortic roots and ascending aortas of Fbn1C1041G/+ mice, further validated in MFS patients.

View Article and Find Full Text PDF

ECM Modifications Driven by Age and Metabolic Stress Directly Promote the Vascular Smooth Muscle Cell Osteogenic Processes.

Arterioscler Thromb Vasc Biol

January 2025

British Heart Foundation Centre of Research Excellence, School of Cardiovascular and Metabolic Medicine & Sciences, King's College London, United Kingdom. (M.W., M.F., R.O., L.S., M.M., C.M.S.).

Background: The ECM (extracellular matrix) provides the microenvironmental niche sensed by resident vascular smooth muscle cells (VSMCs). Aging and disease are associated with dramatic changes in ECM composition and properties; however, their impact on the VSMC phenotype remains poorly studied.

Methods: Here, we describe a novel in vitro model system that utilizes endogenous ECM to study how modifications associated with age and metabolic disease impact the VSMC phenotype.

View Article and Find Full Text PDF

Pulmonary arterial hypertension (PAH) is a rare and potentially fatal condition characterized by progressive increases in blood pressure in the arteries of the lungs. Oral selexipag, approved by the Food and Drug Administration (FDA) in 2015 for the treatment of PAH, targets prostacyclin receptors on pulmonary arterial vascular smooth muscle and endothelial cells to improve blood flow through the lungs and reduce pulmonary vascular resistance. Oral selexipag is effective, but may be discontinued due to factors like side effects, emergency conditions, or inability to take oral medication, potentially leading to severe adverse events, such as rebound pulmonary hypertension and right heart failure.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!