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10.1182/blood-2014-07-586727 http://scihub22266oqcxt.onion/10.1182/blood-2014-07-586727 C4351507!4351507 !25477496     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25477496 &cmd=llinks): Failed to open stream: HTTP request failed! 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Defective release of ? granule and lysosome contents from platelets in mouse Hermansky-Pudlak syndrome models |pdf=|usr=}}{{25477496 }} gab.com Text Defective release of granule and lysosome contents from platelets in mouse Hermansky-Pudlak syndrome models JO: Blood http://www.kidney.de/pget.php?&tw=1&pmid=25477496 #FOAvip Hermansky-Pudlak syndrome (HPS) is characterized by oculocutaneous albinism, bleeding diathesis, and other variable symptoms. The bleeding diathesis has been attributed to ? storage pool deficiency, reflecting the malformation of platelet dense granules. Here, we analyzed agonist-stimulated secretion from other storage granules in platelets from mouse HPS models that lack adaptor protein (AP)-3 or biogenesis of lysosome-related organelles complex (BLOC)-3 or BLOC-1. We show that ? granule secretion elicited by low agonist doses is impaired in all 3 HPS models. High agonist doses or supplemental adenosine 5'-diphosphate (ADP) restored normal ? granule secretion, suggesting that the impairment is secondary to absent dense granule content release. Intravital microscopy following laser-induced vascular injury showed that defective hemostatic thrombus formation in HPS mice largely reflected reduced total platelet accumulation and affirmed a reduced area of ? granule secretion. Agonist-induced lysosome secretion ex vivo was also impaired in all 3 HPS models but was incompletely rescued by high agonist doses or excess ADP. Our results imply that (1) AP-3, BLOC-1, and BLOC-3 facilitate protein sorting to lysosomes to support ultimate secretion; (2) impaired secretion of ? granules in HPS, and to some degree of lysosomes, is secondary to impaired dense granule secretion; and (3) diminished ? granule and lysosome secretion might contribute to pathology in HPS. Twit Text FOAVip Defective release of granule and lysosome contents from platelets in mouse Hermansky-Pudlak syndrome models ????Blood http://www.kidney.de/pget.php?&tw=1&pmid=25477496 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25477496 #FOAvip English Wikipedia <ref>{{Cite pmid|25477496 }}</ref> Defective release of ? granule and lysosome contents from platelets in mouse Hermansky-Pudlak syndrome models #MMPMID25477496 Meng R ; Wu J ; Harper DC ; Wang Y ; Kowalska MA ; Abrams CS ; Brass LF ; Poncz M ; Stalker TJ ; Marks MS Blood 2015[Mar]; 125 (10 ): 1623-32 PMID25477496 show ga Hermansky-Pudlak syndrome (HPS) is characterized by oculocutaneous albinism, bleeding diathesis, and other variable symptoms. The bleeding diathesis has been attributed to ? storage pool deficiency, reflecting the malformation of platelet dense granules. Here, we analyzed agonist-stimulated secretion from other storage granules in platelets from mouse HPS models that lack adaptor protein (AP)-3 or biogenesis of lysosome-related organelles complex (BLOC)-3 or BLOC-1. We show that ? granule secretion elicited by low agonist doses is impaired in all 3 HPS models. High agonist doses or supplemental adenosine 5'-diphosphate (ADP) restored normal ? granule secretion, suggesting that the impairment is secondary to absent dense granule content release. Intravital microscopy following laser-induced vascular injury showed that defective hemostatic thrombus formation in HPS mice largely reflected reduced total platelet accumulation and affirmed a reduced area of ? granule secretion. Agonist-induced lysosome secretion ex vivo was also impaired in all 3 HPS models but was incompletely rescued by high agonist doses or excess ADP. Our results imply that (1) AP-3, BLOC-1, and BLOC-3 facilitate protein sorting to lysosomes to support ultimate secretion; (2) impaired secretion of ? granules in HPS, and to some degree of lysosomes, is secondary to impaired dense granule secretion; and (3) diminished ? granule and lysosome secretion might contribute to pathology in HPS. |Adaptor Protein Complex 3/deficiency/genetics/physiology [MESH] |Adenosine Diphosphate/pharmacology [MESH] |Animals [MESH] |Blood Platelets/*physiology [MESH] |Carrier Proteins/genetics/physiology [MESH] |Cell Degranulation/physiology [MESH] |Disease Models, Animal [MESH] |Guanine Nucleotide Exchange Factors [MESH] |Hermanski-Pudlak Syndrome/*blood/etiology/genetics [MESH] |Humans [MESH] |Intracellular Signaling Peptides and Proteins [MESH] |Lectins/deficiency/genetics/physiology [MESH] |Lysosomes/physiology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |P-Selectin/blood [MESH] |SNARE Proteins/blood [MESH] |Secretory Vesicles/physiology [MESH] |Thrombin/pharmacology [MESH] |Thrombosis/blood/etiology [MESH]Defective release of ? granule and lysosome contents from platelets in(epmc).pdf DeepDyve Pubget Overpricing