GATA-binding protein 1 (GATA1), an important hematopoietic transcription factor, specifically regulates the proliferation and differentiation of erythroid and megakaryoid cells at the transcription level, which maintains the normal development and maturation of these two lineages. The functional structure of GATA1 is composed of one N-terminal transactivation domain (N-TAD) and two zinc fingers (NF and CF). GATA1 is highly conserved in different species. Alteration of GATA1 expression or function will lead to transcriptional disorder of erythrocyte and megakaryocyte related genes, resulting in various clinical phenotypes. This article reviews the molecular structure of GATA1, its transcriptional regulation in erythrocyte and megakaryocyte, and the hereditary hematopoietic regulatory disorders of these two lineages caused by GATA1 mutations.

Objective:To investigate the effect of alogliptin on bone loss in ovariectomized(OVX)mice.Methods:For animal experiments, thirty 8-week-old C57BL/6J female mice were divided into Sham group, OVX group, and OVX+ alogliptin group. OVX+ alogliptin group were administered with alogliptin in a dosage of 20 mg·kg -1·d -1 by gavage, Sham and OVX groups with equivalent saline. After 12 weeks intervention, serum bone anabolism indicators were detected, and Micro CT and HE staining were used to observe and analyze the bone trabecular structure of femur and tibia in mice. For in vitro experiments, bone marrow mesenchymal stem cells(BMSCs)were incubated with 100 μmol/L alogliptin for osteoblast differentiation. Alkaline phosphatase(ALP)and alizarin red S staining were used to determine the ALP activity and mineralization after osteogenic induction and culture. Real-time fluorescence quantitative PCR and Western blot were used to detect mRNA and protein expressions of osteoblast related genes. Results:Alogliptin intervention improved the biochemical indexes of bone anabolism and protected against bone microstructure deterioration to alleviate bone loss in OVX mice. Alogliptin stimulated osteoblast differentiation and elevated expression levels of Runt-related transcription factor 2(Runx2), ALP, osteocalcin, and osterix in in vitro experiments. Conclusion:Alogliptin can alleviate bone loss in OVX mice.

Objective To explore the effect of suledexide on renal injury and podocalyxin expression of podocytes in STZ diabetic desoxycorticosterone acetate (DOCA)-hypertensive rats. Methods Wistar rats were subjected to subcutaneous injection of streptozotocin(STZ), followed by uninephrectomy and subcutaneous administration of DOCA. Diabetic and hypertensive rats were randomly allocated to treatment with sulodexide or a combination of sulodexide and telmisartan for 8 weeks. Blood pressure (BP), 24-hour urinary albumin were measured every 2 weeks. Blood and urinary samples were collected to detect biochemical indexes of plasma and urinary β-acetyl-β-D-glucosaminidase (NAG) at the end of the study. Immunohistochemistry (IHC), RT-PCR and Western blot were performed to examine the expression and distribution of podocalyxin. Results STZ +DOCA-treated rats progressively developed hypertension, albuminuria and hyperglycemia. Hyperlipidemia and hypoinsulinemia were found in diabetic and hypertensive rats compared with controls. Albuminuia was significantly reduced in sulodexide group at week 8 and sulodexide plus telmisartan group at week 6 and week 8. Blood pressure decreased in sulodexide plus telmisartan group. No significant effects on lipid and glucose metabolism were observed in all treated groups. Histopathological index increased in STZ+DOCA-treated rats, but was significantly lower in sulodexide group as well as sulodexide plus telmisartan group. The number of podocytes on glomerular cross-section of the four groups were comparable. Segmental loss and down-regulation of podocalyxin were detected in STZ+DOCA-treated rats, which were greatly attenuated by sulodexinde, meanwhile, combination treatment preserved more podocalyxin expression in glomeruli than sulodexide monotherapy. Conclusion Sulodexide effectively reduces albuminuria, prevents loss of podocyte podocalyxin and alleviates renal damage in STZ diabetic DOCA-hypertensive rats.