Author(s)

Kalev Ingrid, Pechter Ülle, Kõlvald Külli, Aunapuu Marina, Uhlinova Jana, Ots-Rosenberg Mai

Department of Anatomy, Tartu University, Tartu, Estonia.
Department of General and Molecular Pathology, Tartu University, Tartu, Estonia.
Department of Internal Medicine, Tartu University, Tartu, Estonia.

Chronic kidney disease (CKD) is a progressive disease and affects approximately 10% of the population. The major late pathologic feature of CKD is interstitial fibrosis in the kidney characterized by extracellular matrix deposition but in early stage, several profibrotic and proinflammatory cytokines as well as growth factors are expressed. The renin-angiotensin and ET systems both play an important role in the pathogenesis of CKD and the blockade of these systems has been shown to suppress proinflammatory cytokines and to arrest the progression of CKD. We have demonstrated earlier also the renoprotective effect of physical activity on the experimental CKD progression (Pechter et al., 2003). Aim of the study was to investigate the effects of non-drug treatment, physical activity, to the extent of gene expression in experimental CKD and to compare with endothelin receptor blocker (ERB, sitaxentan) and standard nephroprotective drug, angiotensin receptor blocker (ARB, losartan) treatments. Expression of mRNA was assessed by real-time reverse transcription-polymerase chain reaction. CCL2/MCP-1 and nuclear factor-κB (NFκB) gene expression was measured in whole kidneys. Results revealed that CCL2/MCP-1 gene expression (data presented in poster presentation ASN Renal Week 2010, Pechter et al.) was increased in the 5/6 NPX rat kidneys, and the increase was lessened significantly after physical activity and losartan therapy. ERB treatment appeared less effective. Combined ARB and ERB treatment as well as drugs alone or physical therapy prevented the increase in systemic blood pressure, albuminuria and CCL2/MCP-1 as well as NFκB gene expression. We conclude that non-drug and drug treatments both were effective regarding the rate of the progression of experimental CKD measured by physiological and molecular biomarkers of chronic inflammation in kidney tissue.

Remnant Kidney, Gene Transcription, Hypertension, Physical Activity, Renoprotection

Ingrid, K. , Ülle, P. , Külli, K. , Marina, A. , Jana, U. and Mai, O. (2014) CCL2/MCP-1 and NFκB Gene Transcription in Remnant Kidneys after Physical Activity and Renoprotection. World Journal of Cardiovascular Diseases, 4, 244-250. doi: 10.4236/wjcd.2014.45032.