Accumulation of fetal fibronectin mRNAs during the development of rat cardiac hypertrophy induced by pressure overload.

Samuel, Jane‐Lise; Barrieux, A; Dufour, Sylvie; Dubus, Isabelle; Contard, F.; Koteliansky, Victor; Farhadian, Farahnaz; Marotte, F.; Thiéry, Jean Paul; Rappaport, L.

doi:10.1172/jci115492

Cited by 99 publications

(38 citation statements)

References 41 publications

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“…The histochemical data shown in this study indicate that the observed increase in immunodetectable fibronectin was also localized in the fibrotic regions. We (4) and others (22) had previously used in situ hybridization to localize these changes to regions of fibroblast proliferation and showed that fibronectin expression increased before changes in collagen expression, a finding consistent with other models of wound healing. The amount of ang II we used to produce extensive cardiac fibrosis in the L-NAME-treated rats was insufficient to cause similar changes in rats not given L-NAME, suggesting a synergistic effect between L-NAME and ang II on the development of cardiac fibrosis.…”

Section: Discussionsupporting

confidence: 79%

Angiotensin II-induced cardiac fibrosis in the rat is increased by chronic inhibition of nitric oxide synthase.

Hou¹,

Katô²,

Cohen³

et al. 1995

J. Clin. Invest.

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These studies were performed to determine if the effects of angiotensin II infusion on the development of cardiac fibrosis could be modified by the chronic inhibition of nitric oxide synthase activity. NG-nitro-L-arginine-methyl ester (L-NAME) was administered to adult Wistar rats in drinking water (40 mg/kg per d). Although blood pressure was maintained at hypertensive levels after 2 wk, cardiac hypertrophy or fibrosis did not occur. Angiotensin II, given for 3 d at a dose which induced little or no blood pressure elevation and minimal if any fibrosis, caused significant fibrosis when given to a rat pretreated for 2 wk with L-NAME. This marked fibrosis did not occur if angiotensin I was given shortly after L-NAME treatment was begun or briefly after discontinuation of L-NAME. The fibrosis that occurred with combined treatment was characterized by increased immunodetectable fibronectin, the presence of inflammatory cells within interstitial and perivascular regions, and increased steady state mRNA levels for matrix genes and atrial natriuretic protein. The data indicated a regulatory role for nitric oxide in modulating the angiotensin TI-induced cardiac fibrosis and suggest a potentially important autocrine or paracrine role for nitric oxide in fibroblast proliferation. (J.

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Section: Discussionsupporting

confidence: 79%

Angiotensin II-induced cardiac fibrosis in the rat is increased by chronic inhibition of nitric oxide synthase.

Hou¹,

Katô²,

Cohen³

et al. 1995

J. Clin. Invest.

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“…For each transcript, the differential expression is given as the T/N ratio. * P Ͻ 0.05. fetal form, as already described during pressure overload (47,45). Fibronectin was identified using relative RT-PCR analysis with primers located within part of the 3Ј-UTR.…”

Section: Discussionmentioning

confidence: 80%

Heart transplantation changes the expression of distinct gene families

Ngimbous

Bourgeois

Mas

et al. 2001

Physiological Genomics

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We took advantage of the combination of a rat heart transplantation model with a modified differential display RT-PCR method to identify transcriptome changes in the right atria from transplanted compared with native hearts. Based on sequence homology search, the 37 cDNAs differentially displayed both 2 and 7 days posttransplantation were categorized into 7 unknown transcripts, 16 expressed sequence tags (ESTs), and 14 partially or completely characterized genes. The last group cDNAs, validated by relative RT-PCR, belonged to diverse gene families involved in specific metabolisms, protein synthesis, cell signaling, and transcription. Furthermore, we identified differential transcripts corresponding to denervation and fetal gene reexpression. We found coordinate downregulation of genes involved in energy metabolism and protein synthesis regulation, similar to that reported for senescent skeletal muscle. From these transcriptome changes, we propose that heart transplants and senescent muscles share common molecular mechanisms.

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“…The enhanced expression of a ubiquitous SERCA 2 isoform can be related to a shift toward more immature phenotype of smooth muscle cells as previously suggested. 46 The change in SERCA 2b expression in vessels, however, was not associated with an alteration in IP 3 R mRNA level.…”

Section: Discussionmentioning

confidence: 88%

Cellular Distribution of Ca ²⁺ Pumps and Ca ²⁺ Release Channels in Rat Cardiac Hypertrophy Induced by Aortic Stenosis

et al. 1998

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Background-The response of ventricular myocytes to pressure overload is heterogeneous and not spatially coordinated.We investigated whether or not the alterations in SERCA and RyR gene expression are homogeneous within the myocardium. Methods and Results-The cellular distribution of mRNAs and proteins encoding the 2 sarco(endo)plasmic reticulum Ca 2ϩ -ATPase (SERCA) isoforms (SERCA 2a and 2b) and 2 Ca 2ϩ release channels (the ryanodine receptor, RyR, and the IP 3 receptor, IP 3 R) were analyzed by in situ hybridization and immunofluorescence, respectively. Analyses were performed during early (1 and 5 days) and late (1 month) stages of cardiac hypertrophy induced in rat by thoracic aortic stenosis (AS). The results indicated that 1 and 5 days after AS, the cellular distribution of SERCA 2a and RyR2 mRNAs in right ventricle and atrium was similar to controls but the mRNA levels appeared to decrease in some areas of the left ventricle (LV). One month after AS, the distribution of SERCA 2a mRNA and protein became heterogeneous throughout the LV, whereas RyR2 mRNA and protein levels were decreased in a homogeneous manner. SERCA 2b, poorly expressed in both cardiomyocytes and vessels of controls, was increased 4-fold 1 month after AS in coronary arteries only. In both sham (Sh) and AS, SERCA 3 and IP 3 R mRNAs were mainly found in the vessels. Conclusions-In

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Accumulation of fetal fibronectin mRNAs during the development of rat cardiac hypertrophy induced by pressure overload.

Cited by 99 publications

References 41 publications

Angiotensin II-induced cardiac fibrosis in the rat is increased by chronic inhibition of nitric oxide synthase.

Angiotensin II-induced cardiac fibrosis in the rat is increased by chronic inhibition of nitric oxide synthase.

Heart transplantation changes the expression of distinct gene families

Cellular Distribution of Ca ²⁺ Pumps and Ca ²⁺ Release Channels in Rat Cardiac Hypertrophy Induced by Aortic Stenosis

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Accumulation of fetal fibronectin mRNAs during the development of rat cardiac hypertrophy induced by pressure overload.

Cited by 99 publications

References 41 publications

Angiotensin II-induced cardiac fibrosis in the rat is increased by chronic inhibition of nitric oxide synthase.

Angiotensin II-induced cardiac fibrosis in the rat is increased by chronic inhibition of nitric oxide synthase.

Heart transplantation changes the expression of distinct gene families

Cellular Distribution of Ca 2+ Pumps and Ca 2+ Release Channels in Rat Cardiac Hypertrophy Induced by Aortic Stenosis

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Cellular Distribution of Ca ²⁺ Pumps and Ca ²⁺ Release Channels in Rat Cardiac Hypertrophy Induced by Aortic Stenosis