To evaluate a predictive model of microalbuminuria by using anthropometric, clinical and genetic variables in relatives of subjects with diabetic nephropathy.

Sinusoidal endothelial liver cells (SECs) have a key role in the pathophysiology of chronic liver disease. Leptin is an important profibrogenic and proinflammatory cytokine whose expression in sinusoidal endothelial liver has not been documented. The authors studied the potential of rat SECs to express the leptin and leptin receptor genes. Two cell lines of rat SECs were generated from a male rat liver by pronase-collagenase perfusion and dilution cloning. They were characterized according to morphology, ploidy, von Willebrand antigen immunoreactivity, CD31 transcription, matrix metalloproteinase secretion, and pseudocapillary formation. Expression of the leptin and leptin receptor genes was studied using qualitative reverse transcriptase–polymerase chain reaction. Both cell lines fulfilled the accepted criteria for consideration as being derived from the liver sinusoidal endothelium. Confluent monolayers of both cell lines transcribed leptin and leptin receptor genes. This work demonstrated that SECs can transcribe the leptin gene in vitro, cotranscribing with the leptin receptor gene. Leptin production and signaling at this level could be of paramount importance in liver physiopathology; further studies of this issue are warranted because it represents a potential intervention point during chronic liver diseases.

Estrogens play a key role in breast cancer, with 60-70% of the cases expressing estrogen receptors (ERs), which are encoded by the ESR1 gene. CTCFL, a paralogue of the chromatin organizer CTCF, is a potential biomarker of breast cancer, but its expression in this disease is currently controversial. A positive correlation has been reported between CTCFL and ERs in breast tumors and there also exists a coordinated interaction between CTCF and ERs in breast cancer cells. Therefore, there appears to be an association between CTCF, CTCFL and estrogens in breast cancer; however, there has been no report on the effects of estrogens on CTCF and CTCFL expression. The aim of this study was to determine the effect of 17β-estradiol (E2) on the CTCF and CTCFL mRNA expression in the MCF7 breast cancer cell line. the promoter methylation status of CTCFL and data mining for estrogen response elements in promoters of the CTCF and CTCFL genes were also determined. The transcription of CTCF and CTCFL was performed by quantitative polymerase chain reaction (qPCR) and the promoter methylation status of CTCFL was determined by methylation‑specific PCR. The MCF7 cells exhibited basal transcription of CTCF, which was significantly downregulated to 0.68 by 1 µM E2; basal or E2‑regulated transcription of CTCFL was not detected. Under basal conditions, the CTCFL promoter was methylated. Through data mining, an estrogen response element was identified in the CTCF promoter, but no such element was found in CTCFL. These results suggested that estrogens may modulate CTCF expression, although there was no apparent association between ERs and CTCFL.