kidney

Macrophage Cyclooxygenase-2 Protects Against Development of Diabetic Nephropathy

Diabetic nephropathy (DN) is characterized by increased macrophage infiltration, and proinflammatory “M1” macrophages contribute to development of DN. Previous studies by us and others have reported that macrophage cyclooxygenase-2 (COX-2) plays a role in polarization and maintenance of a macrophage tissue reparative “M2” phenotype. We examined the effects of macrophage COX-2 on development of DN in type I diabetes.

Antifibrotic Effects of the Dual CCR2/CCR5 Antagonist Cenicriviroc in Animal Models of Liver and Kidney Fibrosis

Interactions between C-C chemokine receptor types 2 (CCR2) and 5 (CCR5) and their ligands, including CCL2 and CCL5, mediate fibrogenesis by promoting monocyte/macrophage recruitment and tissue infiltration, as well as hepatic stellate cell activation. 

Late Intervention with the Small Molecule BB3 Mitigates Post-ischemic Kidney Injury

Ischemia-reperfusion-mediated acute kidney injury can necessitate renal replacement therapy and is a major cause of morbidity and mortality. We have identified BB3, a small molecule, which when first administered at 24 hr following renal ischemia in rats, improved survival, augmented urine output and reduced the increase in serum creatinine and blood urea nitrogen. 

Proximal tubule-derived colony stimulating factor-1 mediates polarization of renal macrophages and dendritic cells, and recovery in acute kidney injury

Infiltrating cells play an important role in both the development of and recovery from acute kidney injury (AKI). Macrophages and renal dendritic cells are of particular interest because they can exhibit distinctly different functional phenotypes, broadly characterized as proinflammatory (M1) or tissue reparative (M2). 

Inhibition of cyclooxygenase-2 in hematopoietic cells results in salt-sensitive hypertension

Inhibition of prostaglandin (PG) production with either nonselective or selective inhibitors of cyclooxygenase-2 (COX-2) activity can induce or exacerbate salt-sensitive hypertension. This effect has been previously attributed to inhibition of intrinsic renal COX-2 activity and subsequent increase in sodium retention by the kidney.