The results show decrease of frequency of CUS and increase of gain of smooth components after EMDR but only when the session was complete and distress dropped to zero.
A critical player in the dedifferentiation of VSMC are the platelet derived growth factors (PDGFs), which promote reduced contractile gene expression, increased migration and increased proliferation of smooth muscle cells [ 83].
The aortic wall thickening could not be attributed to extra elastic lamellae (Fig. 1F), increased deposition of glycosaminoglycans in the ECM, increased numbers of smooth muscle cells or increased proliferation (supplementary material Fig. S4).
Increased expression of smooth muscle cell growth promoters and decreased expression of growth suppressors confirmed smooth muscle cell proliferation in SHR but not in ACTH.
The increased quantity of smooth muscle in the artery wall could increase the constrictive ability of the artery or the artery wall thickness, either of which could constrict the lumen of the artery, thus reducing blood flow through the vessel.
An increase of airway smooth muscle (ASM) mass due to proliferation and hypertrophy of ASM cells (ASMC) plays an important role in the pathophysiology of airway hyper-responsiveness and remodeling in asthma [ 4, 5].
By further investigating the effects of these factors on MSC gene expression, we found that the change in BGH3 appears to be controlled at the transcriptional level, while the increase in CNN3 may be controlled post-transcriptionally, in contrast to the synergistic increase of the smooth muscle contractile marker, calponin 1 (CNN1), by both cyclic strain and TGF-β1.
Since several early studies have demonstrated the monoclonal type of increase of vascular smooth muscle cells number in atherosclerotic lesions [ 19– 21], a possible mechanism of the focal origin of atherosclerotic plaques may be partially explained by a local damage of cells with high level of mutated mtDNA.
Together, these data demonstrate that the increased response to vagal stimulation in parathion-treated animals was due to increased acetylcholine release, and not to inhibited AChE activity or increased sensitivity of smooth muscle.
Pretreatment of mice with salbutamol abrogates the increased airway resistance in AdS OVA-challenged mice, suggesting that the enhanced resistance is mainly due to increased contractility of smooth muscle.
