Role of angiotensin II type 1 receptor in the regulation of cellular adhesion molecules in atherosclerosis

2001 ◽  
Vol 142 (2) ◽  
pp. 248-253 ◽  
Author(s):  
Abhiram Prasad ◽  
Kwang Kon Koh ◽  
William H. Schenke ◽  
Rita Mincemoyer ◽  
Gyorgy Csako ◽  
...  
1995 ◽  
Vol 65 (12) ◽  
pp. 838-847 ◽  
Author(s):  
A. F. Breidahl ◽  
M. J. Hickey ◽  
A. G. Stewart ◽  
P. G. Hayward ◽  
W. A. Morrison

1999 ◽  
Vol 11 (58) ◽  
pp. 73-93 ◽  
Author(s):  
Zoltan Szekanecz ◽  
Margaret M. Halloran ◽  
Catherine J. Haskell ◽  
Manisha R. Shah ◽  
Peter J. Polverini ◽  
...  

2006 ◽  
Vol 7 (4) ◽  
pp. 297-312 ◽  
Author(s):  
Charles A. Griffis ◽  
Peggy Compton ◽  
Lynn Doering

The psychophysiological phenomenon of pain is of tremendous concern to nurses because of its potential to adversely affect the mental, emotional, and physical health of patients. Increasingly appreciated is the ability of pain to influence immune variables including enumerative and functional measures of leukocyte subsets. In this review, a theoretical model of the role of pain in producing positive changes in the expression of leukocyte cellular adhesion molecules is developed. The model is based on a conceptualization of pain as a perturbing influence on the complex web of neuroendocrine-immune relationships that regulate leukocyte migration. Findings from multiple lines of research are reviewed, including the neurophysiology and psychophysiology of pain, neuroendocrine and proinflammatory cytokine responses to painful stress, animal models linking pain to proinflammatory central immune activation, and pain-specific neurogenic inflammation. Relevant findings are synthesized to develop the physiological pathways from the perspective that pain may alter the balance of this multidirectional system in a proinflammatory direction. Clinical implications and suggestions for further research in the area of painful stress-related inflammation are offered.


Author(s):  
S.L. Erlandsen

Cells interact with their extracellular environments by means of a variety of cellular adhesion molecules (CAM) and surface ligands. In many instances, CAMs interact in a sequential temporal fashion which suggests that these adhesion molecules may occupy or be polarized to various membrane microdomains on the cell surface. Detection of CAMs can be accomplished by a variety of methods including immunofluorescent microscopy and flow cytometry, and by the use of immunocytochemical markers (i.e. colloidal gold) in electron microscopy. The development of high resolution field emission SEM in the mid 1980's and the Autrata modification of the YAG detector for backscatter electron detection at low voltage has greatly facilitated the recognition of colloidal gold probes for detection of surface CAMs. Low voltage FESEM with Bse imaging provides increased resolution of cell surface topography (~3nm at 3-4 keV) which can be observed in 3-dimensions, and simultaneously permits detection/high spatial resolution of immunogold label by atomic number contrast.


2021 ◽  
pp. 1-8
Author(s):  
Mahmood Tavakkoli ◽  
Saeed Aali ◽  
Borzoo Khaledifar ◽  
Gordon A. Ferns ◽  
Majid Khazaei ◽  
...  

<b><i>Background:</i></b> Post-surgical adhesion bands (PSABs) are a common complication after abdominal or pelvic surgeries for different reasons like cancer treatment. Despite improvements in surgical techniques and the administration of drugs or the use of physical barriers, there has only been limited improvement in the frequency of postoperative adhesions. Complications of PSAB are pain, infertility, intestinal obstruction, and increased mortality. The most important molecular mechanisms for the development of PSAB are inflammatory response, oxidative stress, and overexpression of pro-fibrotic molecules such as transforming growth factor β. However, questions remain about the pathogenesis of this problem, for example, the causes for individual differences or why certain tissue sites are more prone to post-surgical adhesions. <b><i>Summary:</i></b> Addressing the pathological causes of PSAB, the potential role of local angiotensin II/angiotensin II type 1 receptors (AngII/AT1R), may help to prevent this problem. <b><i>Key Message:</i></b> The objective of this article was to explore the role of the AngII/AT1R axis potential to induce PSAB and the therapeutic potential of angiotensin receptor blockers in the prevention and treatment of PSAB.


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