Abstract
Stress fibers (SFs) in cells transmit external forces to cell nuclei, altering the DNA structure, gene expression, and cell activity. To determine whether SFs are involved in mechanosignal transduction upon intraluminal pressure, this study investigated the SF direction in smooth muscle cells (SMCs) in aortic tissue and strain in the SF direction. Aortic tissues were fixed under physiological pressure of 120 mmHg. First, we observed fluorescently labeled SFs using two-photon microscopy. It was revealed that SFs in the same smooth muscle layers were aligned in almost the same direction, and the absolute value of the alignment angle from the circumferential direction was 16.8° ± 5.2° (n = 96, mean ± SD). Second, we quantified the strain field in the aortic tissue in reference to photo-bleached markers. It was found in the radial-circumferential plane that the largest strain direction was − 21.3° ± 11.1°, and the zero normal strain direction was 28.1° ± 10.2°. Thus, the SFs in aortic SMCs were not in line with neither the largest strain direction nor the zero strain direction, although their orientation was relatively close to the zero strain direction. These results suggest that SFs in aortic SMCs undergo stretch, but not maximal and transmit the force to nuclei under intraluminal pressure.
Highlights
Hypertension is associated with aortic wall thickening, which occurs as homeostasis to keep circumferential stress in the aortic wall constant (Matsumoto and Hayashi 1996a, 1996b)
In vitro studies have shown that cyclic stretch causes smooth muscle cells (SMCs) to proliferate (Li et al 1997; Song et al 2012) and alter collagen α1 messenger RNA expression (Stanley et al 2000) and fibronectin production rates (Stanley et al 2000)
These results indicate that increased SMC stretch promotes aortic wall hypertrophy in hypertension patients
Summary
Hypertension is associated with aortic wall thickening, which occurs as homeostasis to keep circumferential stress in the aortic wall constant (Matsumoto and Hayashi 1996a, 1996b). In vitro studies have shown that cyclic stretch causes SMCs to proliferate (Li et al 1997; Song et al 2012) and alter collagen α1 messenger RNA (mRNA) expression (Stanley et al 2000) and fibronectin production rates (Stanley et al 2000). These results indicate that increased SMC stretch promotes aortic wall hypertrophy in hypertension patients. These results offer a hypothesis that external forces transmitted to cell nucleus through SFs lead to nuclear deformation
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