Nephropathy in Hypertensive Animals Is Linked to M2 Macrophages and Increased Expression of the YM1/Chi3l3 Protein

Figure 12

Macrophage polarization in the kidneys of 10- to 12-week-old hypertensive mice. The hypertensive stimuli from RAAS, as high levels of AOGEN contributed to macrophage polarization in the kidneys of hypertensive mice with a clear predominance of the M2 phenotype. The high levels of TGF-β1 may be involved in the development of fibrosis. Basal levels of IL-10 do not represent a form of protection against renal fibrosis in the hypertensive animals. In addition, at this stage of hypertension, our data do not support the polarization of macrophages to an M1 phenotype. It seems that the AT1aR in the kidneys from the hypertensive animals were not activated. High levels of AOGEN plus the hypertensive environment contribute to the M2 macrophage polarization. M2 macrophages produced high levels of YM1/Chi3l3 protein (91,89%).