Cleavage of focal adhesion kinase in vascular smooth muscle cells overexpressing membrane-type matrix metalloproteinases

Membrane-type matrix metalloproteinases (MT-MMPs) were initially identified as cell surface activators of MMP-2 (gelatinase A). We have reported that MT1-MMPs and MT3-MMPs are expressed by activated vascular smooth muscle cells (SMCs) and play a role in the regulation of cell function. Overexpression of MT-MMPs results in cell rounding, decreased adherence, and increased migration. Because integrin-mediated cell adhesion regulates these events, we have investigated the functional relationship between MT-MMPs and focal adhesion assembly

Adjusting to Retirement from Sport: Narratives of Former Competitive Rhythmic Gymnasts

This study used narrative inquiry to understand the retirement experiences of rhythmic gymnasts. Eight female former competitive gymnasts (M age = 24.5, SD = 8.33) each participated in four life-history interviews. Following dialogical narrative analysis, three narrative typologies were outlined: Entangled Narrative, Going Forward Narrative, and Making Sense Narrative. The entangled narrative shows an individual with a monological athletic identity, who is unable to develop a new identity following her retirement to the detriment of her well-being, and wishes to return to being a gymnast. The going-forward narrative describes those former gymnasts who were able to develop multiple identities during their gymnastics career, and are now flourishing in their life post-retirement. The making-sense narrative is an emergent narrative, which transcends the previous two narratives. Findings expand narrative research by providing new narrative resources to understand the experience of retirement from gymnastics. These narrative resources might assist gymnasts to expand their narrative repertoire by raising awareness of different narratives available in their culture

Vascular Remodeling in Health and Disease

The term vascular remodeling is commonly used to define the structural changes in blood vessel geometry that occur in response to long-term physiologic alterations in blood flow or in response to vessel wall injury brought about by trauma or underlying cardiovascular diseases.1, 2, 3, 4 The process of remodeling, which begins as an adaptive response to long-term hemodynamic alterations such as elevated shear stress or increased intravascular pressure, may eventually become maladaptive, leading to impaired vascular function. The vascular endothelium, owing to its location lining the lumen of blood vessels, plays a pivotal role in regulation of all aspects of vascular function and homeostasis.5 Thus, not surprisingly, endothelial dysfunction has been recognized as the harbinger of all major cardiovascular diseases such as hypertension, atherosclerosis, and diabetes.6, 7, 8 The endothelium elaborates a variety of substances that influence vascular tone and protect the vessel wall against inflammatory cell adhesion, thrombus formation, and vascular cell proliferation.8, 9, 10 Among the primary biologic mediators emanating from the endothelium is nitric oxide (NO) and the arachidonic acid metabolite prostacyclin [prostaglandin I2 (PGI2)], which exert powerful vasodilatory, antiadhesive, and antiproliferative effects in the vessel wall

Cleavage of focal adhesion kinase in vascular smooth muscle cells overexpressing membrane-type matrix metalloproteinases

none6siMembrane-type matrix metalloproteinases (MT-MMPs) were initially identified as cell surface activators of MMP-2 (gelatinase A). We have reported that MT1-MMPs and MT3-MMPs are expressed by activated vascular smooth muscle cells (SMCs) and play a role in the regulation of cell function. Overexpression of MT-MMPs results in cell rounding, decreased adherence, and increased migration. Because integrin-mediated cell adhesion regulates these events, we have investigated the functional relationship between MT-MMPs and focal adhesion assembly.noneT. Shofuda; K. Shofuda; N. Ferri; R.D. Kenagy; E.W. Raines; A.W. ClowesT., Shofuda; K., Shofuda; Ferri, Nicola; R. D., Kenagy; E. W., Raines; A. W., Clowe