FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2120709903> ?p ?o ?g. }

• W2120709903 abstract "The vascular system develops through two distinct pathways known as vasculogenesis and angiogenesis. The former involves formation of vascular networks from endothelial progenitor cells (Kasmeyer et al. 2009), while angiogenesis is the extension of new blood vessels from pre-existing ones (Robinson et al. 2009). The establishment and optimal functioning of the vasculature is an essential component throughout the body and the ovary is no exception. Blood vessel growth is tightly regulated requiring the timely balance between proand antiangiogenic growth factors as well as the complex, intimate interplay between endothelial cells and various other cell types (e.g. immune cells and pericytes). In this Research Front on ovarian angiogenesis, we present four reviews and one original article that reveal the latest research and current hypotheses on the key stages of vascular development in the ovary. Remarkably little was known about how the vasculature in the fetal ovary is formed, until recently. In the first paper of this Research Front, the latest insights are highlighted byMcFee and Cupp (2012). Intriguingly, ovarian vasculature in the embryo appears to develop through a vasculogenic process rather than the typical angiogenesis that occurs in embryonic testes. Moreover, the vascular patterning is preferentially aligned along the neuronal network template and thus could be influenced by neuronal growth factors (Anderson et al. 2002). McFee and Cupp (2012) also suggest that the ability of germ cell/oocytes to proliferate, develop and form primordial follicles is potentially influenced by fetal ovarian medulla blood supply since these cells lack a direct blood supply. Indeed, follicle assembly initially originates near to the medullary vasculature (Sawyer et al. 2002). This would imply that the inappropriate development of an ovarian vasculature could result in improper prenatal folliculogenesis. This could then adversely affect fertility of both women and animals. The VEGF system is very complex with the existence of numerous proand anti-angiogenic isoforms, receptors and signalling partners (Gabhann and Popel 2008).McFee and Cupp (2012) provide a scholarly account of their importance in the regulation of fetal ovarian development. They speculate that the temporal differences in expression of pro-angiogenic ‘a’ and anti-angiogenic ‘b’ VEGFA isoforms might explain the different patterns of vascularisation in the fetal ovary and testes (McFee andCupp 2012). Interestingly, Qiu et al. (2012) recently showed that overexpression of VEGF165b reduced follicular development and number of ovulations and more importantly, this was associatedwith lower fertility inmice. Collectively, this further emphasises that optimal ovarian function requires an appropriate balance between proand anti-angiogenic factors. It is well established that hypoxia-induced expression of VEGFA plays a pivotal role in stimulating angiogenesis during tumour development. However, the exact role of hypoxia in ovarian angiogenesis has remained elusive for a long time. In the second review of this Research Front, Meidan et al. (2012) discuss the role of the transcription factor, hypoxia inducible factor 1p/b (HIF1p/b), which is critical for ovulation in mice (Kim et al. 2009). The current evidence indicates that HIF1pis upregulated and translocates to the nucleus of luteinising granulosa cell during the ovulatory window although this upregulation is only short-lived. It is likely that, at least in part, the LH surge upregulates the HIF1p in luteinising follicular cells (van den Driesche et al. 2008). This feature of HIF1p regulation could be unique to the ovary. It is also increasingly apparent that any induction of HIF1pstimulates VEGFA expression in luteal cells (Zhang et al. 2011). What is less well known is the role of hypoxia and/or HIF1pin the regulation of FGF2. This certainly requires investigation since FGF2 and HIF1p expression profiles are closelymatched in the bovine CL (Robinson et al. 2007; Nishimura and Okuda 2010). Furthermore, it is becoming increasing apparent that FGF2 is a key factor controlling endothelial cell sprouting during the follicle-luteal transition in cattle (Laird et al. 2012). Accurate measurement of tissue hypoxia is challenging and will continue to hinder the elucidation of the role hypoxia plays in ovarian angiogenesis. The use of novel, live imaging positron emission tomography (PET) technologies using biomarkers such as F-labelled fluoromisonidazole (F-MISO) as used in tumour biology (Mendichovszky and Jackson 2011) will help to address this challenge. Furthermore, such technologiesmight increase our understanding of the role of hypoxia in disorders such as luteal deficiency. It has been long-recognised that ovulation has numerous characteristics of an inflammatory response. However, the role of immune cells in the regulation of ovarian angiogenesis has been neglected, until recently and these findings are highlighted by Shirasuna et al. (2012) in the third review. While there are some definite species differences, there is a pool of evidence that immune cells (e.g. neutrophils, macrophages and/or lymphocytes) infiltrate into the developing CL. This is likely due to CSIRO PUBLISHING" @default.
• W2120709903 created "2016-06-24" @default.
• W2120709903 creator A5010628153 @default.
• W2120709903 date "2013-01-01" @default.
• W2120709903 modified "2023-09-26" @default.
• W2120709903 title "The critical importance of ovarian angiogenesis" @default.
• W2120709903 cites W1899116820 @default.
• W2120709903 cites W1972365140 @default.
• W2120709903 cites W1991380281 @default.
• W2120709903 cites W2022286005 @default.
• W2120709903 cites W2053609204 @default.
• W2120709903 cites W2057515598 @default.
• W2120709903 cites W2059155698 @default.
• W2120709903 cites W2064530674 @default.
• W2120709903 cites W2077771962 @default.
• W2120709903 cites W2093096968 @default.
• W2120709903 cites W2100145954 @default.
• W2120709903 cites W2104514705 @default.
• W2120709903 cites W2107583561 @default.
• W2120709903 cites W2116801378 @default.
• W2120709903 cites W2125250856 @default.
• W2120709903 cites W2128205037 @default.
• W2120709903 cites W2138153686 @default.
• W2120709903 cites W2146076252 @default.
• W2120709903 cites W2147427742 @default.
• W2120709903 cites W2148902771 @default.
• W2120709903 cites W2160394750 @default.
• W2120709903 cites W2165386218 @default.
• W2120709903 cites W2169002696 @default.
• W2120709903 cites W2171649027 @default.
• W2120709903 cites W4236174308 @default.
• W2120709903 cites W4243589323 @default.
• W2120709903 doi "https://doi.org/10.1071/rdv25n2_ed" @default.
• W2120709903 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23445820" @default.
• W2120709903 hasPublicationYear "2013" @default.
• W2120709903 type Work @default.
• W2120709903 sameAs 2120709903 @default.
• W2120709903 citedByCount "7" @default.
• W2120709903 countsByYear W21207099032013 @default.
• W2120709903 countsByYear W21207099032014 @default.
• W2120709903 countsByYear W21207099032016 @default.
• W2120709903 countsByYear W21207099032017 @default.
• W2120709903 countsByYear W21207099032021 @default.
• W2120709903 countsByYear W21207099032022 @default.
• W2120709903 crossrefType "journal-article" @default.
• W2120709903 hasAuthorship W2120709903A5010628153 @default.
• W2120709903 hasBestOaLocation W21207099031 @default.
• W2120709903 hasConcept C104317684 @default.
• W2120709903 hasConcept C134018914 @default.
• W2120709903 hasConcept C145103041 @default.
• W2120709903 hasConcept C169760540 @default.
• W2120709903 hasConcept C201750760 @default.
• W2120709903 hasConcept C203014093 @default.
• W2120709903 hasConcept C2777663904 @default.
• W2120709903 hasConcept C2778324911 @default.
• W2120709903 hasConcept C2780394083 @default.
• W2120709903 hasConcept C28328180 @default.
• W2120709903 hasConcept C502942594 @default.
• W2120709903 hasConcept C54355233 @default.
• W2120709903 hasConcept C60781801 @default.
• W2120709903 hasConcept C86803240 @default.
• W2120709903 hasConcept C95444343 @default.
• W2120709903 hasConceptScore W2120709903C104317684 @default.
• W2120709903 hasConceptScore W2120709903C134018914 @default.
• W2120709903 hasConceptScore W2120709903C145103041 @default.
• W2120709903 hasConceptScore W2120709903C169760540 @default.
• W2120709903 hasConceptScore W2120709903C201750760 @default.
• W2120709903 hasConceptScore W2120709903C203014093 @default.
• W2120709903 hasConceptScore W2120709903C2777663904 @default.
• W2120709903 hasConceptScore W2120709903C2778324911 @default.
• W2120709903 hasConceptScore W2120709903C2780394083 @default.
• W2120709903 hasConceptScore W2120709903C28328180 @default.
• W2120709903 hasConceptScore W2120709903C502942594 @default.
• W2120709903 hasConceptScore W2120709903C54355233 @default.
• W2120709903 hasConceptScore W2120709903C60781801 @default.
• W2120709903 hasConceptScore W2120709903C86803240 @default.
• W2120709903 hasConceptScore W2120709903C95444343 @default.
• W2120709903 hasLocation W21207099031 @default.
• W2120709903 hasLocation W21207099032 @default.
• W2120709903 hasOpenAccess W2120709903 @default.
• W2120709903 hasPrimaryLocation W21207099031 @default.
• W2120709903 hasRelatedWork W1008271900 @default.
• W2120709903 hasRelatedWork W189320039 @default.
• W2120709903 hasRelatedWork W1972839104 @default.
• W2120709903 hasRelatedWork W2008951881 @default.
• W2120709903 hasRelatedWork W2015522187 @default.
• W2120709903 hasRelatedWork W2027403533 @default.
• W2120709903 hasRelatedWork W2047060427 @default.
• W2120709903 hasRelatedWork W2065032881 @default.
• W2120709903 hasRelatedWork W2132936161 @default.
• W2120709903 hasRelatedWork W2146878122 @default.
• W2120709903 hasRelatedWork W2151842614 @default.
• W2120709903 hasRelatedWork W2172633275 @default.
• W2120709903 hasRelatedWork W2355157319 @default.
• W2120709903 hasRelatedWork W2357869597 @default.
• W2120709903 hasRelatedWork W2385395343 @default.
• W2120709903 hasRelatedWork W2385884095 @default.
• W2120709903 hasRelatedWork W2470214321 @default.
• W2120709903 hasRelatedWork W2476332147 @default.
• W2120709903 hasRelatedWork W3028811579 @default.

• next