Thrombomodulin Induces a Quiescent Phenotype and Inhibits Migration in Vascular Smooth Muscle Cells In Vitro

Bass, Heather M.; Beard, Richard S.; Byeong, J.; Yuan, Sarah Y.; Nelson, Peter R.

doi:10.1016/j.avsg.2015.10.002

Cited by 3 publications

(1 citation statement)

References 14 publications

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“…ECIS is a real-time, medium throughput assay, widely used to quantify adherent cell behavior and contraction 13–16 . ECIS has been used previously to study SMC growth and behavior in wound-healing and migration assays 17–19 . We thus opted to use ECIS as a novel, quantitative strategy to analyze the contractile responses of vascular SMC.…”

Section: Introductionmentioning

confidence: 99%

Impaired smooth muscle cell contractility as a novel concept of abdominal aortic aneurysm pathophysiology

Bogunovic

Meekel

Micha

et al. 2019

Sci Rep

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Ruptured abdominal aortic aneurysms (AAA) are associated with overall mortality rates up to 90%. Despite extensive research, mechanisms leading to AAA formation and advancement are still poorly understood. Smooth muscle cells (SMC) are predominant in the aortic medial layer and maintain the wall structure. Apoptosis of SMC is a well-known phenomenon in the pathophysiology of AAA. However, remaining SMC function is less extensively studied. The aim of this study is to assess the in vitro contractility of human AAA and non-pathologic aortic SMC. Biopsies were perioperatively harvested from AAA patients (n = 21) and controls (n = 6) and clinical data were collected. Contractility was measured using Electric Cell-substrate Impedance Sensing (ECIS) upon ionomycin stimulation. Additionally, SMC of 23% (5 out of 21) of AAA patients showed impaired maximum contraction compared to controls. Also, SMC from patients who underwent open repair after earlier endovascular repair and SMC from current smokers showed decreased maximum contraction vs. controls (p = 0.050 and p = 0.030, respectively). Our application of ECIS can be used to study contractility in other vascular diseases. Finally, our study provides with first proof that impaired SMC contractility might play a role in AAA pathophysiology.

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