title: Transforming growth factor-beta expression in cardiovascular organs in stroke-prone spontaneously hypertensive rats with the development of hypertension.
abstract: Transforming growth factor (TGF)-beta activity is involved in several cardiovascular diseases owing to its effects on the growth of vascular smooth muscle cells and induction of extracellular matrix formation. We evaluated expression of TGF-beta in cardiovascular organs from stroke-prone spontaneously hypertensive rats (SHR-SP) which show severe cardiovascular damages with the development of hypertension. Twelve-week-old Wistar-Kyoto (WKY)/Izm rats and SHR-SP/Izm were loaded with 1% salt for 4 weeks. Aorta, heart and kidney were removed and evaluated histologically by hematoxylin-eosin staining. Expression of TGF-beta1 mRNA was evaluated by reverse transcription and polymerase chain reaction analysis in mRNA extracted with oligo dT-cellulose. Expression of TGF-beta1 protein was evaluated by Western blot analysis and immunohistochemical study in renal cortex. Whereas expression of TGF-beta1 mRNA was detected only in the heart of SHR-SP before salt loading, it was detected in the aorta, left ventricle of heart and renal cortex from both rat strains, and it was stronger in the renal cortex of SHR-SP than in the renal cortex of WKY rats. Expression of TGF-beta1 protein was markedly higher in the renal cortex of SHR-SP than in the renal cortex of WKY rats after salt loading. TGF-beta was localized at glomeruli and capillary arteries in the renal cortex, and immunostaining was stronger in SHR-SP than in WKY rats. Expression of TGF-beta1 was increased in glomeruli and capillaries of the renal cortex with the development of hypertension in SHR-SP. These results implicate TGF-beta in the renal damage observed in hypertension.
authors.affiliation: Second Department of Internal Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan.
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Tahira
authors.forename: Noboru
authors.initials: N
authors.lastname: Fukuda
authors.forename: Morito
authors.initials: M
authors.lastname: Endo
authors.forename: Ryo
authors.initials: R
authors.lastname: Suzuki
authors.forename: Yukihiro
authors.initials: Y
authors.lastname: Ikeda
authors.forename: Hiroto
authors.initials: H
authors.lastname: Takagi
authors.forename: Koichi
authors.initials: K
authors.lastname: Matsumoto
authors.forename: Katsuo
authors.initials: K
authors.lastname: Kanmatsuse
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002319:Cardiovascular System / Q000378:metabolism* / Q000473:pathology; D020022:Genetic Predisposition to Disease; D006973:Hypertension / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007150:Immunohistochemistry; D007672:Kidney Cortex / Q000378:metabolism; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR / Q000235:genetics / Q000378:metabolism*; D011921:Rats, Inbred WKY; D020521:Stroke / Q000235:genetics*; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism*
chemical_list: D012333:RNA, Messenger; D016212:Transforming Growth Factor beta