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  • 1
    Publication Date: 2008-02-22
    Description: Ischaemia of the heart, brain and limbs is a leading cause of morbidity and mortality worldwide. Hypoxia stimulates the secretion of vascular endothelial growth factor (VEGF) and other angiogenic factors, leading to neovascularization and protection against ischaemic injury. Here we show that the transcriptional coactivator PGC-1alpha (peroxisome-proliferator-activated receptor-gamma coactivator-1alpha), a potent metabolic sensor and regulator, is induced by a lack of nutrients and oxygen, and PGC-1alpha powerfully regulates VEGF expression and angiogenesis in cultured muscle cells and skeletal muscle in vivo. PGC-1alpha-/- mice show a striking failure to reconstitute blood flow in a normal manner to the limb after an ischaemic insult, whereas transgenic expression of PGC-1alpha in skeletal muscle is protective. Surprisingly, the induction of VEGF by PGC-1alpha does not involve the canonical hypoxia response pathway and hypoxia inducible factor (HIF). Instead, PGC-1alpha coactivates the orphan nuclear receptor ERR-alpha (oestrogen-related receptor-alpha) on conserved binding sites found in the promoter and in a cluster within the first intron of the VEGF gene. Thus, PGC-1alpha and ERR-alpha, major regulators of mitochondrial function in response to exercise and other stimuli, also control a novel angiogenic pathway that delivers needed oxygen and substrates. PGC-1alpha may provide a novel therapeutic target for treating ischaemic diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arany, Zoltan -- Foo, Shi-Yin -- Ma, Yanhong -- Ruas, Jorge L -- Bommi-Reddy, Archana -- Girnun, Geoffrey -- Cooper, Marcus -- Laznik, Dina -- Chinsomboon, Jessica -- Rangwala, Shamina M -- Baek, Kwan Hyuck -- Rosenzweig, Anthony -- Spiegelman, Bruce M -- P30 DK040561/DK/NIDDK NIH HHS/ -- P30 DK040561-12/DK/NIDDK NIH HHS/ -- R01 DK054477/DK/NIDDK NIH HHS/ -- England -- Nature. 2008 Feb 21;451(7181):1008-12. doi: 10.1038/nature06613.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA. zarany1@partners.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18288196" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Hypoxia ; Cells, Cultured ; Gene Expression Regulation ; Hypoxia-Inducible Factor 1/metabolism ; Ischemia/*metabolism ; Mice ; Mice, Transgenic ; Muscle, Skeletal/metabolism ; *Neovascularization, Physiologic ; Oxygen/metabolism ; Receptors, Estrogen/metabolism ; Trans-Activators/deficiency/genetics/*metabolism ; Transcription Factors ; Transgenes/genetics ; Vascular Endothelial Growth Factor A/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2008-02-02
    Description: In the mammalian ovary, progressive activation of primordial follicles from the dormant pool serves as the source of fertilizable ova. Menopause, or the end of female reproductive life, occurs when the primordial follicle pool is exhausted. However, the molecular mechanisms underlying follicle activation are poorly understood. We provide genetic evidence that in mice lacking PTEN (phosphatase and tensin homolog deleted on chromosome 10) in oocytes, a major negative regulator of phosphatidylinositol 3-kinase (PI3K), the entire primordial follicle pool becomes activated. Subsequently, all primordial follicles become depleted in early adulthood, causing premature ovarian failure (POF). Our results show that the mammalian oocyte serves as the headquarters of programming of follicle activation and that the oocyte PTEN-PI3K pathway governs follicle activation through control of initiation of oocyte growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reddy, Pradeep -- Liu, Lian -- Adhikari, Deepak -- Jagarlamudi, Krishna -- Rajareddy, Singareddy -- Shen, Yan -- Du, Chun -- Tang, Wenli -- Hamalainen, Tuula -- Peng, Stanford L -- Lan, Zi-Jian -- Cooney, Austin J -- Huhtaniemi, Ilpo -- Liu, Kui -- New York, N.Y. -- Science. 2008 Feb 1;319(5863):611-3. doi: 10.1126/science.1152257.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biochemistry and Biophysics, Umea University, SE-901 87 Umea, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18239123" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Follicular Atresia ; Mice ; Mice, Transgenic ; Oocytes/cytology/growth & development/*physiology ; Organ Size ; Ovarian Follicle/cytology/*physiology ; Ovary/anatomy & histology/physiology ; Ovulation ; PTEN Phosphohydrolase/genetics/*physiology ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Primary Ovarian Insufficiency/physiopathology ; Protein Kinases/metabolism ; Ribosomal Protein S6/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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