title: Atrial expression of the CCN1 and CCN2 proteins in chronic heart failure.
abstract: Previous studies have reported the upregulation of CCN proteins early after acute heart injury. The aim of the present work was to evaluate the expression of the CCN1 and CCN2 proteins and their regulation by angiotensin II in the atrial myocardium of a chronically failing heart. Male adult mice were subjected to ligation of the left coronary artery to produce myocardial infarction (the MI group), and 16 of them were treated for 12 weeks with the AT1 receptor antagonist telmisartan (the MI-Tel group). Sham-operated mice served as controls. The expression of proteins was evaluated by immunohistochemistry 12 weeks after the operation. In shamoperated mice, stainings for CCN1 and CCN2 proteins were positive within atrial cardiomyocytes. CCN1-positive reaction revealed diffused cytoplasmic localization, while CCN2 was present mainly within the perinuclear cytoplasm. CCN1 was upregulated in the MI group, while CCN2 remained at basal level. Telmisartan prevented the upregulation of CCN1 and decreased CCN2 level. We compared the experimental data with the expression of CCN1 and CCN2 proteins in human right atrial appendages. We found an inverse, but not significant, relation between the level of either protein and the left ventricular ejection fraction. This suggests a similar atrial regulation of CCN1 and CCN2 expression also in humans. We conclude that in the murine atria, CCN1 and CCN2 proteins are expressed constitutively. In chronic heart failure, CCN proteins tend to be upregulated, which may be related to the action of angiotensin II.
authors.affiliation: Department of General and Experimental Pathology, Medical University of Bialystok, Mickiewicza Str. 2c, 15-222 Bialystok, Poland. tomasz.bonda@umb.edu.pl
authors.forename: Tomasz A
authors.initials: TA
authors.lastname: Bonda
authors.forename: Karol A
authors.initials: KA
authors.lastname: Kamiński
authors.forename: Magdalena
authors.initials: M
authors.lastname: Dziemidowicz
authors.forename: Sergey
authors.initials: S
authors.lastname: Litvinovich
authors.forename: Marcin
authors.initials: M
authors.lastname: Kożuch
authors.forename: Tomasz
authors.initials: T
authors.lastname: Hirnle
authors.forename: Iwona
authors.initials: I
authors.lastname: Dmitruk
authors.forename: Lech
authors.initials: L
authors.lastname: Chyczewski
authors.forename: Maria M
authors.initials: MM
authors.lastname: Winnicka
mesh_terms: D000818:Animals; D020517:Atrial Appendage / Q000737:chemistry / Q000378:metabolism* / Q000473:pathology; D002908:Chronic Disease; D055513:Connective Tissue Growth Factor / Q000032:analysis / Q000096:biosynthesis*; D055515:Cysteine-Rich Protein 61 / Q000032:analysis / Q000096:biosynthesis*; D006325:Heart Atria / Q000737:chemistry / Q000378:metabolism* / Q000473:pathology; D006333:Heart Failure / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D006801:Humans; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism / Q000473:pathology
chemical_list: C501848:CCN1 protein, human; C491850:CCN1 protein, mouse; C526317:CCN2 protein, human; C526318:CCN2 protein, mouse; D055515:Cysteine-Rich Protein 61; D055513:Connective Tissue Growth Factor