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Left ventricular periostin gene expression is associated with fibrogenesis in experimental renal insufficiency
Virva Pohjolainen1, Jaana Rysä, Juha Näpänkangas
1Department of Pharmacology and Toxicology, Institute of Biomedicine, University of Oulu, Biocentre Oulu, Oulu, Finland.
Insights
Periostin is re-expressed in chronic renal insufficiency (CRI), contributing to cardiac fibrosis. Elevated blood pressure likely triggers this response in the heart.
Area of Science:
- Nephrology
- Cardiology
- Molecular Biology
Background:
- Cardiovascular diseases are a leading cause of death in patients with chronic renal insufficiency (CRI).
- Left ventricular hypertrophy (LVH), fibrosis, and calcification are common cardiac manifestations of CRI.
- Periostin, a matricellular protein, is implicated in fibrogenesis and calcification during tissue remodeling.
Purpose of the Study:
- To investigate the role of periostin in CRI-induced left ventricular hypertrophy (LVH).
- To explore the factors influencing periostin re-expression in the context of chronic kidney disease.
Main Methods:
- Rats underwent 5/6 nephrectomy (NX) to induce CRI.
- Following disease progression, rats received high-calcium, high-phosphate, or paricalcitol treatment.
- Cardiac tissue and blood samples were analyzed for periostin gene expression, inflammatory markers, and fibrotic proteins. LV periostin expression was also studied under pressure overload conditions.
Main Results:
- Chronic renal insufficiency (CRI) led to a 6.5-fold increase in left ventricular (LV) periostin mRNA.
- Periostin was localized to inflammatory and fibrotic areas in the heart.
- LV periostin mRNA levels correlated significantly with impaired kidney function biomarkers, LVH, fibrogenesis markers, and systolic blood pressure.
Conclusions:
- Periostin plays a role in cardiac fibrotic remodeling associated with CRI.
- Periostin re-expression in CRI is linked to fibrotic and inflammatory lesions.
- Elevated blood pressure is a likely trigger for periostin activation in CRI.
Background:
Cardiovascular diseases are the most important cause of death in patients with impaired kidney function. Left ventricular hypertrophy (LVH), cardiac interstitial fibrosis and cardiovascular calcifications are characteristic of chronic renal insufficiency (CRI). Periostin is a fibrogenesis- and calcification-related matricellular protein re-expressed in adult tissues undergoing remodelling in response to pathological stimuli. The role of periostin in CRI-induced LVH is unknown.
Methods:
Rats were 5/6-nephrectomized (NX), and after 15 weeks of disease progression high-calcium, high-phosphate or paricalcitol treatment was given for 12 weeks. Cardiac tissue and blood samples were taken to study periostin gene expression and to determine factors contributing to its reactivation, respectively. Left ventricular (LV) periostin expression was also examined in response to angiotensin II or arginine(8)-vasopressin (AVP)-induced pressure overload and in spontaneously hypertensive rats.
Results:
CRI resulted in a 6.5-fold increase in LV periostin messenger RNA (mRNA) levels. Positive extracellular immunostaining for periostin was detected in areas of infiltrated inflammatory cells and fibrotic lesions. There was a significant correlation between LV periostin mRNA levels and plasma biomarkers of impaired kidney function, LVH, fibrogenesis-related proteins osteopontin and osteoactivin, and anti-calcific matrix Gla protein. Moreover, LV periostin gene expression in CRI correlated positively with systolic blood pressure (BP) and was activated rapidly in response to angiotensin II or AVP infusions.
Conclusions:
Periostin is involved in fibrotic cardiac remodelling in CRI. The re-expression of periostin is localized to the fibrotic and inflammatory lesions and is most likely the consequence of elevated BP.
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