Bioscience Reports最新文献

Loss of cardiomyocyte-specific Adhesion G Protein Coupled Receptor G1 (ADGRG1/GPR56) promotes pressure overload-induced heart failure. 心肌细胞特异性粘附G蛋白偶联受体G1（ADGRG1/GPR56）的缺失会促进压力过载引起的心力衰竭。

IF 4 3区生物学

Bioscience Reports Pub Date : 2024-09-12 DOI: 10.1042/bsr20240826

Jeanette Einspahr,Heli Xu,Rajika Roy,Nikki Dietz,Jacob Melchior,Jhansi Raja,Rhonda L Carter,Xianhua Piao,Douglas Tilley

{"title":"Loss of cardiomyocyte-specific Adhesion G Protein Coupled Receptor G1 (ADGRG1/GPR56) promotes pressure overload-induced heart failure.","authors":"Jeanette Einspahr,Heli Xu,Rajika Roy,Nikki Dietz,Jacob Melchior,Jhansi Raja,Rhonda L Carter,Xianhua Piao,Douglas Tilley","doi":"10.1042/bsr20240826","DOIUrl":"https://doi.org/10.1042/bsr20240826","url":null,"abstract":"Adhesion G protein coupled receptors (AGPCRs), containing large N-terminal ligand-binding domains for environmental mechano-sensing, have been increasingly recognized to play important roles in numerous physiologic and pathologic processes. However, their impact on the heart, which undergoes dynamic mechanical alterations in healthy and failing states, remains understudied. ADGRG1 (formerly known as GPR56) is widely expressed, including in skeletal muscle where it was previously shown to mediate mechanical overload-induced muscle hypertrophy, thus we hypothesized that it could impact the development of cardiac dysfunction and remodeling in response to pressure overload. In this study, we generated a cardiomyocyte (CM)-specific ADGRG1 knockout mouse model, which, although not initially displaying features of cardiac dysfunction, does develop increased systolic and diastolic LV volumes and internal diameters over time. Notably, when challenged with chronic pressure overload, CM-specific ADGRG1 deletion accelerates cardiac dysfunction, concurrent with blunted CM hypertrophy, enhanced cardiac inflammation and increased mortality, suggesting that ADGRG1 plays an important role in the early adaptation to chronic cardiac stress. Altogether, this study provides an important proof-of-concept that targeting CM-expressed AGPCRs may offer a new avenue for regulating the development of heart failure.","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":null,"pages":null},"PeriodicalIF":4.0,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142191217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Axonal neurotransmitter release in the regulation of myelination. 调节髓鞘化的轴突神经递质释放

IF 3.8 3区生物学

Bioscience Reports Pub Date : 2024-09-04 DOI: 10.1042/BSR20231616

Rafael Almeida, Katy Marshall-Phelps

{"title":"Axonal neurotransmitter release in the regulation of myelination.","authors":"Rafael Almeida, Katy Marshall-Phelps","doi":"10.1042/BSR20231616","DOIUrl":"https://doi.org/10.1042/BSR20231616","url":null,"abstract":"Myelination of axons is a key determinant of fast action potential propagation, axonal health and circuit function. Previously considered a static structure, it is now clear that myelin is dynamically regulated in response to neuronal activity in the CNS. However, how activity-dependent signals are conveyed to oligodendrocytes remains unclear. Here we review the potential mechanisms by which neurons could communicate changing activity levels to myelin, with a focus on the accumulating body of evidence to support activity-dependent vesicular signalling directly onto myelin sheaths. We discuss recent in vivo findings of activity-dependent fusion of neurotransmitter vesicles from non-synaptic axonal sites, and how modulation of this vesicular fusion regulates the stability and growth of myelin sheaths. We also consider the potential mechanisms by which myelin could sense and respond to axon-derived signals to initiate remodelling, and the relevance of these adaptations for circuit function. We propose that axonal vesicular signalling represents an important and underappreciated mode of communication by which neurons can transmit activity-regulated signals to myelinating oligodendrocytes and, potentially, more broadly to other cell types in the CNS.","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142124723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Interaction with IP6K1 supports pyrophosphorylation of substrate proteins by the inositol pyrophosphate 5-InsP7. 与 IP6K1 相互作用，支持肌醇焦磷酸 5-InsP7 对底物蛋白质进行焦磷酸化。

IF 3.8 3区生物学

Bioscience Reports Pub Date : 2024-09-04 DOI: 10.1042/BSR20240792

Rashna Bhandari, Aisha Hamid, Jayashree S Ladke, Akruti Shah, Shubhra Ganguli, Monisita Pal, Arpita Singh

{"title":"Interaction with IP6K1 supports pyrophosphorylation of substrate proteins by the inositol pyrophosphate 5-InsP7.","authors":"Rashna Bhandari, Aisha Hamid, Jayashree S Ladke, Akruti Shah, Shubhra Ganguli, Monisita Pal, Arpita Singh","doi":"10.1042/BSR20240792","DOIUrl":"https://doi.org/10.1042/BSR20240792","url":null,"abstract":"Inositol pyrophosphates (PP-InsPs) are a sub-family of water soluble inositol phosphates that possess one or more diphosphate groups. PP-InsPs can transfer their β-phosphate group to a phosphorylated Ser residue to generate pyrophosphorylated Ser. This unique post-translational modification occurs on Ser residues that lie in acidic stretches within an intrinsically disordered protein sequence. Serine pyrophosphorylation is dependent on the presence of Mg2+ ions, but does not require an enzyme for catalysis. The mechanisms by which cells regulate PP-InsP-mediated pyrophosphorylation are still unknown. We performed mass spectrometry to identify interactors of IP6K1, an enzyme responsible for the synthesis of the PP-InsP 5-InsP7. Interestingly, IP6K1 interacted with several proteins that are known to undergo 5-InsP7-mediated pyrophosphorylation, including the nucleolar proteins NOLC1, TCOF and UBF1, and AP3B1, the β subunit of the AP3 adaptor protein complex. The IP6K1 interactome also included CK2, a protein kinase that phosphorylates Ser residues prior to pyrophosphorylation. We observe the formation of a protein complex between IP6K1, AP3B1, and the catalytic α-subunit of CK2, and show that disrupting IP6K1 binding to AP3B1 lowers its in vivo pyrophosphorylation. We propose that assembly of a substrate-CK2-IP6K complex would allow for coordinated pre-phosphorylation and pyrophosphorylation of the target serine residue, and provide a mechanism to regulate this enzyme-independent modification.","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142124724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Integration of clotting and fibrinolysis: central role of platelets and factor XIIIa. 凝血和纤维蛋白溶解的整合：血小板和因子 XIIIa 的核心作用。

IF 3.8 3区生物学

Bioscience Reports Pub Date : 2024-08-30 DOI: 10.1042/BSR20240332

Irina Patalakh, Olga Revka, Agata Gołaszewska, Natalia Bielicka, Tomasz Misztal

{"title":"Integration of clotting and fibrinolysis: central role of platelets and factor XIIIa.","authors":"Irina Patalakh, Olga Revka, Agata Gołaszewska, Natalia Bielicka, Tomasz Misztal","doi":"10.1042/BSR20240332","DOIUrl":"https://doi.org/10.1042/BSR20240332","url":null,"abstract":"The aim of this study was to establish the role of platelets and activated factor XIIIa (FXIIIa) in the structuring of the fibrin network as well as to clarify the effect of network compaction on clot lysis.  Turbidimetry was used for the one-stage clotting test where PFP is regarded as single factor-deficient plasma (platelets as lacking factor) and autologous PRP as deficiency corrected plasma. Structural features of the developed and subsequently lysed fibrin network, formed under static and flow conditions, were visualized by confocal microscopy. Thrombin-initiated plasma clotting revealed changes in the shape of the absorption curve, more pronounced in the presence of platelets. These changes correlate with the transformation of the fibrin scaffold during clot maturing. With the combined action of platelets, thrombin and Ca2+, plasma clotting passes through two phases: initial formation of a platelet-fibrin network (first peak in the polymerization curve), and then the compaction of fibrin, driven by FXIIIa (the second peak) which can be further modulate by the contractile action of platelets. These structural changes, mediated by platelets and FXIIIa, have been shown to determine subsequent clot lysis.  Platelet aggregates serve as organizing centers that determine the distribution of fibrin in clot volume. The openwork structure of the platelet-transformed fibrin provides the necessary prerequisites for its timely lysis. The revealed aspects of the interaction of platelets and FXIIIa, which accompanies the maturation of a fibrin clot, may lead to new approaches in the pharmacological correction of disorders associated with both thrombotic episodes and bleeding tendency.","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Retraction: Extensive mechanical tension promotes annulus fibrosus cell senescence through suppressing cellular autophagy. 撤回：广泛的机械张力通过抑制细胞自噬促进环状纤维肌细胞衰老

IF 3.8 3区生物学

Bioscience Reports Pub Date : 2024-08-28 DOI: 10.1042/BSR-2019-0163_RET