scholarly journals Compromised cardiac performance and remodeling in collagen type VI deficient mice after myocardial infarction

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Daniel John Luther ◽  
Patricia E. Shamhart ◽  
Vaghan Ohanyan ◽  
Cheryl M. Hodnichak ◽  
James T. Miller ◽  
...  
2009 ◽  
Vol 64 (3) ◽  
pp. 329-334 ◽  
Author(s):  
W. Dinh ◽  
L. Bansemir ◽  
R. Füth ◽  
W. Nickl ◽  
J.-P. Stasch ◽  
...  

2021 ◽  
Vol 22 (2) ◽  
pp. 722
Author(s):  
Yukino Ogura ◽  
Kazuko Tajiri ◽  
Nobuyuki Murakoshi ◽  
DongZhu Xu ◽  
Saori Yonebayashi ◽  
...  

Neutrophils are recruited into the heart at an early stage following a myocardial infarction (MI). These secrete several proteases, one of them being neutrophil elastase (NE), which promotes inflammatory responses in several disease models. It has been shown that there is an increase in NE activity in patients with MI; however, the role of NE in MI remains unclear. Therefore, the present study aimed to investigate the role of NE in the pathogenesis of MI in mice. NE expression peaked on day 1 in the infarcted hearts. In addition, NE deficiency improved survival and cardiac function post-MI, limiting fibrosis in the noninfarcted myocardium. Sivelestat, an NE inhibitor, also improved survival and cardiac function post-MI. Flow cytometric analysis showed that the numbers of heart-infiltrating neutrophils and inflammatory macrophages (CD11b+F4/80+CD206low cells) were significantly lower in NE-deficient mice than in wild-type (WT) mice. At the border zone between intact and necrotic areas, the number of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive apoptotic cells was lower in NE-deficient mice than in WT mice. Western blot analyses revealed that the expression levels of insulin receptor substrate 1 and phosphorylation of Akt were significantly upregulated in NE-knockout mouse hearts, indicating that NE deficiency might improve cardiac survival by upregulating insulin/Akt signaling post-MI. Thus, NE may enhance myocardial injury by inducing an excessive inflammatory response and suppressing Akt signaling in cardiomyocytes. Inhibition of NE might serve as a novel therapeutic target in the treatment of MI.


2021 ◽  
Vol 6 (4) ◽  
pp. S338-S339
Author(s):  
M. Tepel ◽  
S. J. L. Bakker ◽  
O. Thaunat ◽  
S. Nagarajah ◽  
F. Genovese ◽  
...  

Blood ◽  
1995 ◽  
Vol 86 (5) ◽  
pp. 1740-1748 ◽  
Author(s):  
G Klein ◽  
CA Muller ◽  
E Tillet ◽  
ML Chu ◽  
R Timpl

Collagen type VI, which forms characteristic microfibrillar structures, is assembled from three individual alpha(VI) chains that form a short triple helix and two adjacent globular domains. Expression of all three alpha (VI) collagen chains in the human bone marrow (BM) microenvironment could be detected by chain-specific antibodies in tissue sections and in the adherent stromal layer of long-term BM cultures. In functional studies, collagen type VI was shown to be a strong adhesive substrate for various hematopoietic cell lines and light-density BM mononuclear cells. The adhesive site within the molecule seems to be restricted to the triple helical domain of all three alpha (VI) chains, because individual alpha (VI) chains were not active in the attachment assays. Adhesion of the hematopoietic cell lines to collagen VI was dose-dependent and could be inhibited by heparin. Although the triple helix contains several RGD sequences, adhesion of the hematopoietic cell types to collagen VI could be blocked neither by RGD-containing peptides nor by a neutralizing antibody to the beta 1 integrin subunit. In combination with an antiadhesive substrate, the binding properties of collagen VI could be downregulated. These data suggest that this collagen type may play an important role in the adhesion of hematopoietic cells within the BM microenvironment.


2003 ◽  
Vol 41 (6) ◽  
pp. 170-171
Author(s):  
Maria A. Cavasin ◽  
Ai-Li Yu ◽  
Shreevidya Menon ◽  
Xiao-Ping Yang

PLoS ONE ◽  
2017 ◽  
Vol 12 (5) ◽  
pp. e0177132 ◽  
Author(s):  
Michal Entin-Meer ◽  
Lena Cohen ◽  
Einat Hertzberg-Bigelman ◽  
Ran Levy ◽  
Jeremy Ben-Shoshan ◽  
...  

2010 ◽  
Vol 28 (11) ◽  
pp. 1507-1514 ◽  
Author(s):  
Dianne H. Murray ◽  
Peter G. Bush ◽  
Ivan J. Brenkel ◽  
Andrew C. Hall

2019 ◽  
Vol 70 (1) ◽  
pp. e819
Author(s):  
Signe Holm Nielsen ◽  
Raj Uchila ◽  
Mohammed Eslam ◽  
Mette Juul Nielsen ◽  
Diana Leeming ◽  
...  

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