Cathepsin G is associated with atheroma formation in human carotid artery

Legedz, Liliana; Randon, Jacques; Sessa, Carmine; Baguet, Jean-Philippe; Feugier, Patrick; Cerutti, Catherine; McGregor, John L.; Bricca, Giampiero

doi:10.1097/00004872-200401000-00025

Cited by 34 publications

(31 citation statements)

References 22 publications

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“…Several clinical trials have demonstrated the benefits of AII blockade using anti-hypertensive drugs in reducing acute cardiovascular events, independent of blood pressure reduction [20][21][22] . There are at least 2 receptors for AII present in atheroma, angiotensin receptor type 1 (ATR1) 23) and 2 (ATR2) 24) . Signalling via both receptors has been reported to regulate MMP expression with most studies suggesting ATR1 mediates MMP up-regulation 18) .…”

Section: Introductionmentioning

confidence: 99%

Involvement of Angiotensin II Type 1 and 2 Receptors in Gelatinase Regulation in Human Carotid Atheroma <i>in vitro </i>

Clancy

Koblar

Golledge

2016

JAT

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Section: Introductionmentioning

confidence: 99%

Involvement of Angiotensin II Type 1 and 2 Receptors in Gelatinase Regulation in Human Carotid Atheroma <i>in vitro </i>

Clancy

Koblar

Golledge

2016

JAT

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“…This finding is in line with previous studies showing the expression of angiotensinogen in several arterial beds. [10][11][12][13] Because it is difficult to acquire normal human arterial tissue, we compared the results obtained from atheroma lesions (ATH) to nearby macroscopically intact arterial tissue (MIT). 2 In addition, the importance of using paired ATH and MIT samples from the same patients is that it reduces clinical and demographic variabilities among individuals and increases the statistical power of differential gene expression.…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Analysis Reveals Novel Transcription Factors Associated With Renin–Angiotensin–Aldosterone System in Human Atheroma

2016

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Abstract-Despite the well-known role of the renin-angiotensin-aldosterone system (RAAS) in atheroma, its global local organization is poorly understood. In this study, we used transcriptomic meta-analysis to reveal the local transcriptional organization and regulation of 37 extended RAAS (extRAAS) genes in atheroma. Expression analysis and hierarchical clustering were done on extRAAS genes in 32 paired early and advanced atherosclerotic lesions. Contrary to receptorcoding transcripts, multiple angiotensin-metabolizing enzymes showed higher expression in advance, in comparison to early lesions. Interestingly, similar results were obtained from GEO data sets containing human (n=839) and mouse (n=18) atherosclerotic samples, but different from normal human (n=11) arterial tissues. The expression and coordination patterns were then used to construct transcriptional maps of extRAAS, displaying favored pathways in atheroma. Three coexpression modules (M1, M2, and M3) with >80% reproducibility across human atheroma data sets were identified. M1 and M3 contained angiotensin-metabolizing enzymes transcripts, whereas M2 contained proatherogenic receptorcoding transcripts. Interestingly, M1 and M2 were negatively correlated. A total of 21 transcription factors with enriched binding sites in the promoters of coordinated genes were extracted, among which IRF5, MAX, and ETV5 showed significant positive correlations with M1, but negative correlations with M2. However, ETS1 and SMAD1 transcripts were positively correlated to receptor-coding genes in M2. Despite sharing some similarities in extRAAS organization with kidney and adipose, atheroma showed specific correlations between extRAAS and transcription factors. In conclusion, our transcriptional map helps in designing more efficient treatments for atherosclerosis. In addition, the identified transcription factors provide a basis for the discovery of atheroma-specific modulators of extRAAS.

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“…Thus, we can assume the possibility of formation of angiotensin II from angiotensinogen with cathepsin G participation at the CoCl 2 action which contributes to the development of hypertensive changes. Overexpression of cathepsin G also may lead to decreased number of differentiated smooth muscle cells, to the lower amount of angiotensin 1 receptor in atheroma [34]. Cathepsin G activation in heart can result in myocyte necrosis and increased fibrosis [15].…”

Section: Discussionmentioning

confidence: 99%

The activities of endothelial elastase and cathepsin G in rats at oxidative stress caused by heavy metals salts

Starodub¹,

Samokhina²

2013

ABC

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CoCl 2 introduction increased cathepsin G activity in the heart and liver as well as endothelial elastase (EEl) in kidney that indicated the development of destructive processes. CoCl 2 introduction decreased EEl and cathepsin G activities in blood serum and cathepsin G in lungs. HgCl 2 injection decreased EEl in blood serum, heart, liver, kidney and cathepsin G in blood serum. These decreasing of proteinases activities may be caused by cytotoxic effects of heavy metals and/or the inclusion of these proteases in the destructive processes and absence of their synthesis and/or release.

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Cathepsin G is associated with atheroma formation in human carotid artery

Cited by 34 publications

References 22 publications

Involvement of Angiotensin II Type 1 and 2 Receptors in Gelatinase Regulation in Human Carotid Atheroma <i>in vitro </i>

Involvement of Angiotensin II Type 1 and 2 Receptors in Gelatinase Regulation in Human Carotid Atheroma <i>in vitro </i>

Transcriptomic Analysis Reveals Novel Transcription Factors Associated With Renin–Angiotensin–Aldosterone System in Human Atheroma

The activities of endothelial elastase and cathepsin G in rats at oxidative stress caused by heavy metals salts

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