Cytomegalovirus infection of human kidney cells in vitro

Cytomegalovirus infection of human kidney cells in vitro. To study which structures of a kidney allograft are the main targets for cytomegalovirus (CMV), human glomerular epithelial and mesangial cells, as well as tubular epithelial and endothelial cells were isolated by steel meshes of different pore sizes and enzymatic treatments. The various cultured cell types were characterized by morphology and specific antibodies. Human CMV was inoculated onto cell monolayers using two different culture methods: conventional tissue culture and rapid shell vial culture. To analyze whether CMV had a direct effect on the immunologic properties of kidney parenchymal cells, MHC class I and class II antigen expression was estimated before and after the infection. CMV infected all kidney cells identically. All cells expressed class I strongly after the infection, but they were class I positive prior to infection. Class II antigens were not expressed on the cell surface either before or after the infection. In conclusion, human kidney cells of glomerular, tubular and vascular origin were all infected by CMV without any difference. CMV had no significant direct effects on the antigenic properties of the cells

MANF is indispensable for the proliferation and survival of pancreatic beta-cells

All forms of diabetes mellitus (DM) are characterized by the loss of functional pancreatic β cell mass, leading to insufficient insulin secretion. Thus, identification of novel approaches to protect and restore β cells is essential for the development of DM therapies. Mesencephalic astrocyte-derived neurotrophic factor (MANF) is an endoplasmic reticulum (ER)-stress-inducible protein, but its physiological role in mammals has remained obscure. We generated MANF-deficient mice that strikingly develop severe diabetes due to progressive postnatal reduction of β cell mass, caused by decreased proliferation and increased apoptosis. Additionally, we show that lack of MANF in vivo in mouse leads to chronic unfolded protein response (UPR) activation in pancreatic islets. Importantly, MANF protein enhanced β cell proliferation in vitro and overexpression of MANF in the pancreas of diabetic mice enhanced β cell regeneration. We demonstrate that MANF specifically promotes β cell proliferation and survival, thereby constituting a therapeutic candidate for β cell protection and regeneration.Peer reviewe