Cardiac gene expression and systemic cytokine profile are complementary in a murine model of post-ischemic heart failure

Lachtermacher, Stephan; Esporcatte, Bruno L. B.; Montalvão, Fabricio; Costa, Patrícia; Rodrigues, Deivid C.; Belém, Luciano; Rabischoffisky, Arnaldo; Neto, Hugo Caire Castro-Faria; Vasconcellos, Ricardo José de Holanda; Iacobaş, Sanda; Iacobaş, Dumitru A.; Hj, Dohmann; Spray, David C.; Goldenberg, Regina Coeli dos Santos; Carvalho, Antônio Carlos Campos de

doi:10.1590/s0100-879x2010007500014

Cited by 24 publications

(26 citation statements)

References 36 publications

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“…typically found to be increased in the kidney in progressive renal disease, are the major source of fibrogenic cytokines including IL-6 and TGF-␤ (38). Furthermore, in the post-MI setting the infarcted heart can be a source of systemic cytokines (3,17,27) that could accelerate the local renal inflammatory and fibrosis processes. Higher plasma IL-6 and C-reactive protein levels have been demonstrated in postacute-MI patients with impaired renal function than those without (37).…”

Section: Discussionmentioning

confidence: 99%

“…The inflammatory cells are a source of various cytokines, such as IL-6, TNF-␣, IL-1␤, and transforming growth factor (TGF)-␤ (11,39), which are involved in the initial stages of postischemic wound healing and eventually lead to fibrosis/scar formation. The post-MI inflammatory response is also likely to be systemic, as evidenced by increased circulating levels of cytokines/inflammatory markers in both human and experimental models (3,17,27).…”

mentioning

confidence: 99%

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Myocardial infarction impairs renal function, induces renal interstitial fibrosis, and increases renal KIM-1 expression: implications for cardiorenal syndrome

Lekawanvijit

Kompa

Zhang

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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Progressive decline in renal function coexists with myocardial infarction (MI); however, little is known about its pathophysiology. This study aimed to systematically identify post-MI renal changes (functional, histological, and molecular) over time in a rat MI model and examine potential mechanisms that may underlie these changes. Rats were randomized into three groups: nonoperated, sham, and MI. Cardiac and renal function was assessed before death at 1, 4, 8, 12, and 16 wk with tissues collected for histological, protein, and gene studies. Tail-cuff blood pressure was lower in MI than sham and nonoperated animals only at 1 wk (P < 0.05). Systolic function was reduced (P < 0.0001) while heart/body weight and left ventricle/body weight were significantly greater in MI animals at all time points. Glomerular filtration rate decreased following MI at 1 and 4 wk (P < 0.05) but not at 8 and 12 wk and then deteriorated further at 16 wk (P = 0.052). Increased IL-6 gene and transforming growth factor (TGF)-β protein expression as well as macrophage infiltration in kidney cortex was detected at 1 wk (P < 0.05). Renal cortical interstitial fibrosis was significantly greater in MI animals from 4 wk, while TGF-β bioactivity (phospho-Smad2) was upregulated at all time points. The degree of fibrosis increased and was maximal at 16 wk. In addition, kidney injury molecule-1-positive staining in the tubules was more prominent in MI animals, maximal at 1 wk. In conclusion, renal impairment occurs early post-MI and is associated with hemodynamic and structural changes in the kidney possibly via activation of the Smad2 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Myocardial infarction impairs renal function, induces renal interstitial fibrosis, and increases renal KIM-1 expression: implications for cardiorenal syndrome

Lekawanvijit

Kompa

Zhang

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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“…Chew et al reported that the overexpression of TL1A induces apoptosis in endothelial cells, resulting in a reduction in MVD (20). TL1A has been found to be significantly upregulated in chronically ischaemic myocardial tissue (21). TL1A mRNA has otherwise been shown to be upregulated in human circulating endothelial progenitor cells from old vs. young human volunteers (22).…”

Section: Discussionmentioning

confidence: 99%

Involvement of TL1A and DR3 in induction of ischaemia and inflammation in urinary bladder dysfunction in the elderly

et al. 2012

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Abstract. Benign prostatic hyperplasia often causes intravesical obstruction in elderly men; however, the processes of aging and bladder outlet obstruction independently evoke alterations in the structure and function of the bladder. These changes lead to lower urinary tract symptoms; however, it is difficult to separate the effects of prostatic obstruction on the bladder from those of aging. Nevertheless, few studies have focused on elucidating the pathophysiological mechanisms in the aged bladder. Bladder dysfunction due to detrusor instabitliy (caused by old age) is considered to be associated with chronic ischaemia and inflammation. The aim of this study was to explore the role of tumour necrosis factor (TNF)-like ligand 1A (TL1A) and death-domain receptor (DR)3 in the ischaemic and inflammatory process of aged bladder dysfunction. Sixteen bladder tissue samples collected from patients with urothelial tumours of the bladder were divided into two groups according to age: group 1 (controls, n=8) and group 2 (aged group, n=8). Urodynamic examinations were preformed before radical cystectomy. The full-thickness bladder tissues were obtained at least 5 cm away from the margin of the tumours. The mRNA expression levels of TL1A, DR3, von Willebrand factor (vWF), interleukin (IL)-6 and nerve growth factor (NGF) in the two groups were determined using real-time reverse transcription-PCR and the protein expression levels of TL1A, DR3 and p65 were determined by western blot analysis. The TL1A and DR3 mRNA and protein expression levels of the aged bladders were upregulated compared to the control group (p<0.05). Compared to the control, the mRNA expression levels of vWF in the aged bladder tissues were markedly lower (p<0.01); however, the mRNA expression levels of IL-6 were significantly higher in the aged bladder tissues (p<0.01) compared to the control. No significant difference in NGF mRNA expression between the two groups was detected (p>0.05). In conclusion, the aged bladder was associated with ischaemic and inflammatory alterations in comparison to the control group. TL1A and DR3 may play an important role in the pathophysiological process of the aged bladder. IntroductionA variety of changes in bladder function have been described during aging in humans and other species. Symptoms in the lower urinary tract are more prevalent among the elderly. Clinical urodynamic studies have demonstrated that aging is related to reduced bladder capacity, increased uninhibited contractions, decreased urinary flow rate, diminished urethral pressure profile (particularly in women) and increased postvoid residual urine volume (1). In particular, the aging bladder may be described as manifesting detrusor overactivity, impaired contractility or a combination of both.Several factors have been thought to play a role in the voiding dysfunction in the elderly, including detrusor fibrosis and consequent impairment of contractility (2), deposition and cross-linking of collagen and elastin, and the loss of acetylcholinesterase-positive ner...

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“…In mouse models of ischemic CMP, the expression of cytokines, IgM, and IgG were increased 3-fold in the post-ischemic state compared to controls. 38 This association between myocardial cell death and immune system activation may indicate a major pathogenic role in the evolution of disease.…”

Section: Antibody Production and Heart Failurementioning

confidence: 99%

The Role of B-Cells in Heart Failure

Cordero‐Reyes

Youker

Torre‐Amione

2013

Methodist DeBakey Cardiovascular Journal

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Cardiac gene expression and systemic cytokine profile are complementary in a murine model of post-ischemic heart failure

Cited by 24 publications

References 36 publications

Myocardial infarction impairs renal function, induces renal interstitial fibrosis, and increases renal KIM-1 expression: implications for cardiorenal syndrome

Myocardial infarction impairs renal function, induces renal interstitial fibrosis, and increases renal KIM-1 expression: implications for cardiorenal syndrome

Involvement of TL1A and DR3 in induction of ischaemia and inflammation in urinary bladder dysfunction in the elderly

The Role of B-Cells in Heart Failure

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