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The expression and new functions of reproductive hormones in organs beyond hypothalamus-pituitary-gonad axis have been reported. So far, there is no report about the protective effects of GnRH analogue to hippocampal neurons suffering from ischemia-reperfusion injury. Middle cerebral artery occlusion model together with TUNEL staining were made in vivo and oxygen-glucose deprivation model together with double staining of Annexin V/PI with flow cytometer were made in vitro to observe the anti-apoptotic effects of GnRH analogue to hippocampal neurons after ischemia-reperfusion injury. The results found that the number of TUNEL positive pyramidal neurons in CA1 region in GnRH analogue experiment group was less than that in control group in vivo; the percentage of apoptotic neurons in GnRH analogue experiment group was less than that in control group in vitro. These findings suggested that pretreatment with certain concentration of GnRH analogue could attenuate apoptosis of hippocampal neurons. GnRH analogue has the protective effects to neurons.

Studies indicated that many tissues could express FSH. New functions of FSH have been recognized beyond reproduction regulation. However, no report has been made about the expression and function of FSH in rat spinal cord. Double-labeled immunofluorescence stain and in situ hybridization were used to study the co-localization of FSH with its receptor and co-localization of FSH with GnRH receptor in rat spinal cord. Spinal cord ischemia injury models were built, TUNEL stain and Fas immunostaining were made to observe the anti-apoptotic effects of FSH to neurons induced by spinal cord ischemia injury. The results found that some neurons and glias of rat spinal cord showed both FSH immunoreactivity and FSH mRNA positive signals; not only FSH and its receptor but also FSH and GnRH receptor co-located in cells of both gray matter and white matter; treatment with certain concentration of FSH before ischemia-reperfusion injury, less TUNEL positive cells and Fas positive cells were found in motor neurons of ventral gray matter in FSH experiment group than that in control group. These suggested that rat spinal cord could express FSH, it is also a target organ of FSH; FSH might exert functions through its receptor by paracrine or autocrine effects; GnRH in spinal cord might regulate FSH positive neurons through GnRH receptor; FSH might inhibit ischemia induced neuron apoptosis by down-regulating Fas expression in spinal cord.

This document is a retraction notice for an article titled "TNFα Promotes Glioblastoma A172 Cell Mitochondrial Apoptosis via Augmenting Mitochondrial Fission and Repression of MAPK–ERK–YAP Signaling Pathways." The retraction is due to concerns about the duplication of images from other unrelated articles in Figures 1, 2, 3, 4, 5, and 6 of the original article. The authors did not respond to queries or provide an explanation for the duplicated images. The retracted article will remain online but will be digitally watermarked as "Retracted." [Extracted from the article]

Background and objective: The present study was designed to explore the roles of mitochondrial fission and MAPK–ERK–YAP signaling pathways and to determine their mutual relationship in TNFα-mediated glioblastoma mitochondrial apoptosis.Materials and methods: Cellular viability was measured via TUNEL staining, MTT assays, and Western blot. Immunofluorescence was performed to observe mitochondrial fission. YAP overexpression assays were conducted to observe the regulatory mechanisms of MAPK–ERK–YAP signaling pathways in mitochondrial fission and glioblastoma mitochondrial apoptosis.Results: The results in our present study indicated that TNFα treatment dose dependently increased the apoptotic rate of glioblastoma cells. Functional studies confirmed that TNFα-induced glioblastoma apoptosis was attributable to increased mitochondrial fission. Excessive mitochondrial fission promoted mitochondrial dysfunction, as evidenced by decreased mitochondrial potential, repressed ATP metabolism, elevated ROS synthesis, and downregulated antioxidant factors. In addition, the fragmented mitochondria liberated cyt-c into the cytoplasm/nucleus where it activated a caspase-9-involved mitochondrial apoptosis pathway. Furthermore, our data identified MAPK–ERK–YAP signaling pathways as the primary molecular mechanisms by which TNFα modulated mitochondrial fission and glioblastoma apoptosis. Reactivation of MAPK–ERK–YAP signaling pathways via overexpression of YAP neutralized the cytotoxicity of TNFα, attenuated mitochondrial fission, and favored glioblastoma cell survival.Conclusion: Overall, our data highlight that TNFα-mediated glioblastoma apoptosis stems from increased mitochondrial fission and inactive MAPK–ERK–YAP signaling pathways, which provide potential targets for new therapies against glioblastoma. [ABSTRACT FROM AUTHOR]