Abstract

The aim of the present study was to investigate the expression of NELIN and SM22α in lower extremity varicose vein tissue, and their association with varicose veins. Tissue samples were collected from 18 patients with lower extremity varicose veins for the experimental group, while normal great saphenous vein tissue was reserved during coronary artery bypass surgery from 14 patients for the controls. Reverse transcription polymerase chain reaction (RT-PCR) analysis was applied to detect the mRNA expression levels of NELIN and SM22α, while immunohistochemical techniques were used to detect the protein expression levels in the normal and abnormal veins. RT-PCR results revealed that the mRNA expression levels of NELIN and SM22α in the experimental group decreased significantly when compared with the control group (P<0.01). In the two groups, immunohistochemical staining demonstrated that NELIN and SM22α were primarily expressed in the cytoplasm of smooth muscle cells, and the expression quantity decreased significantly in the experimental group when compared with the control group (P<0.05). The low expression of SM22α in the primary lower limb varicose vein tissue indicated that the vascular smooth muscle cell layer had transformed from a contractile to a secretory phenotype, which may have resulted in the remodeling of the vein walls and the occurrence of varicose veins. Therefore, NELIN and SM22α were demonstrated to play a key role in the development of varicosity.

Highlights

  • Vascular smooth muscle cells (VSMCs) are a highly specialized type of cell, whose primary functions in mature animals include contraction (1) and the production of matrix compo-Key words: varicose veins, NELIN, SM22α, phenotypic transition, vascular smooth muscle cell nents of the blood vessel wall (2)

  • Reverse transcription polymerase chain reaction (RT‐PCR) analysis revealed that the mRNA expression levels of NELIN in the VSMCs were significantly decreased in the experimental group (0.2867±0.1025) when compared with the control group (0.4221±0.220; P

  • As shown in a previous study, VSMCs cultivated in vitro change from a contractile to a synthetic phenotype following four subcultures, with the symbol of phenotypic transition being a clear reduction in SM22α expression in the VSMCs (14)

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Summary

Introduction

Vascular smooth muscle cells (VSMCs) are a highly specialized type of cell, whose primary functions in mature animals include contraction (1) and the production of matrix compo-. VSMCs exhibit a variety of phenotypes at different developmental stages, under different pathophysiological conditions or normal conditions, depending on the anatomical location of the vessels (4). Previous studies have aimed to distinguish between the two phenotypes of VSMCs, the spindle‐shaped ‘contractile’ and epithelioid‐shaped ‘synthetic’ phenotypes (5). Varicose veins exhibit thickened vessel walls, as a result of the dysregulation of the synthesis of extracellular matrix proteins in SMCs (6). The phenotypic modulation of SMCs can alter extracellular matrix metabolism (7), and the etiology and physiopathology of varicose disorders include venous wall remodeling associated with abnormalities of SMCs and extracellular matrix (8)

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