AGE-RELATED SMOOTH MUSCLE FORMATION IN PELVIC CONNECTIVE TISSUE

Alteration of VSMC (vascular smooth-muscle cell) physiology is associated with the development of atherosclerosis and restenosis. We hypothesize that aging up-regulates the expression of p16INK4a in VSMCs, which may increase the susceptibility of blood vessels to vascular occlusive diseases. Aortic VSMCs were obtained from young and aged mice. Cells from aged mice grew more slowly than those from their younger counterparts. Progression of cell cycle in response to serum stimulation was significantly inhibited in those cells with aging, as determined by FACS after propidium iodide staining. A significant up-regulation of p16INK4a (2.5-fold, P=0.0012) was found in VSMC from aged animals using gene arrays. The up-regulation of this gene was further confirmed by quantitative RT–PCR (reverse transcription–PCR) and Western-blot experiments. Immunostaining for p16INK4a confirmed that aortas from aged mice contained more p16INK4a+ SMA (smooth-muscle cell actin)+ cells than aortas from young animals (26.79±2.45 versus 7.06±1.44, P=0.00027, n=4). In conclusion, we have shown that aging up-regulates the expression of p16INK4a in VSMC in both cultures and arteries. The increase in p16INK4a in the vasculature with aging may modify VSMC's response to post-injury stress and therefore accelerate the development of age-related cardiovascular diseases.

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Assessment of the protein quality of the smooth muscle myofibrillar and connective tissue proteins of chicken gizzard

Poultry Science ◽

10.1093/ps/77.5.770 ◽

1998 ◽

Vol 77 (5) ◽

pp. 770-779 ◽

Cited By ~ 3

Author(s):

C.G. Zarkadas ◽

S.A. Maloney

Keyword(s):

Smooth Muscle ◽

Connective Tissue ◽

Protein Quality ◽

Chicken Gizzard

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Age-related loss of proliferative activity of human vascular smooth muscle cells in culture

Mechanisms of Ageing and Development ◽

10.1016/s0047-6374(99)00042-1 ◽

1999 ◽

Vol 110 (1-2) ◽

pp. 49-55 ◽

Cited By ~ 30

Author(s):

Antonio Ruiz-Torres ◽

Ana Gimeno ◽

José Melón ◽

Luis Mendez ◽

Francisco J. Muñoz ◽

...

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cells ◽

Vascular Smooth Muscle Cells ◽

Proliferative Activity ◽

Muscle Cells ◽

Cells In Culture ◽

Age Related

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Connective tissue growth factor and vascular endothelial growth factor from airway smooth muscle interact with the extracellular matrix

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00287.2005 ◽

2006 ◽

Vol 290 (1) ◽

pp. L153-L161 ◽

Cited By ~ 32

Author(s):

Janette K. Burgess ◽

Qi Ge ◽

Maree H. Poniris ◽

Sarah Boustany ◽

Stephen M. Twigg ◽

...

Keyword(s):

Extracellular Matrix ◽

Vascular Endothelial Growth Factor ◽

Smooth Muscle ◽

Growth Factor ◽

Connective Tissue ◽

Airway Smooth Muscle ◽

Connective Tissue Growth Factor ◽

Tissue Growth ◽

Vascular Endothelial ◽

Endothelial Growth Factor

Airway remodeling describes the structural changes that occur in the asthmatic airway that include airway smooth muscle hyperplasia, increases in vascularity due to angiogenesis, and thickening of the basement membrane. Our aim in this study was to examine the effect of transforming growth factor-β on the release of connective tissue growth factor and vascular endothelial growth factor from human airway smooth muscle cells derived from asthmatic and nonasthmatic patients. In addition we studied the immunohistochemical localization of these cytokines in the extracellular matrix after stimulating bronchial rings with transforming growth factor-β. Connective tissue growth factor and vascular endothelial growth factor were released from both cell types and colocalized in the surrounding extracellular matrix. Prostaglandin E2 inhibited the increase in connective tissue growth factor mRNA but augmented the release of vascular endothelial growth factor. Matrix metalloproteinase-2 decreased the amount of connective tissue growth factor and vascular endothelial growth factor, but not fibronectin deposited in the extracellular matrix. This report provides the first evidence that connective tissue growth factor may anchor vascular endothelial growth factor to the extracellular matrix and that this deposition is decreased by matrix metalloproteinase-2 and prostaglandin E2. This relationship has the potential to contribute to the changes that constitute airway remodeling, therefore providing a novel focus for therapeutic intervention in asthma.

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