Opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy lossResearch in Context

Background: The mechanism behind an increased risk of recurrent pregnancy loss (RPL) remains largely unknown. In our previous study, we identified that inter-α-trypsin inhibitor heavy chain 4 (ITI-H4) is highly expressed at a modified molecular weight of 36 kDa in serum derived from RPL patients. Ye...
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Autor*in:	Lan Li [verfasserIn] Bum-Chae Choi [verfasserIn] Ji Eun Ryoo [verfasserIn] Sang-Jin Song [verfasserIn] Chang-Zhu Pei [verfasserIn] Kwang Yul Lee [verfasserIn] Jinyoung Paek [verfasserIn] Kwang-Hyun Baek [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Übergeordnetes Werk:	In: EBioMedicine - Elsevier, 2015, 37(2018), Seite 535-546
Übergeordnetes Werk:	volume:37 ; year:2018 ; pages:535-546

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.ebiom.2018.10.029

Katalog-ID:	DOAJ072299843

Internformat


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520			\|a Background: The mechanism behind an increased risk of recurrent pregnancy loss (RPL) remains largely unknown. In our previous study, we identified that inter-α-trypsin inhibitor heavy chain 4 (ITI-H4) is highly expressed at a modified molecular weight of 36 kDa in serum derived from RPL patients. Yet, the precise molecular mechanism and pathways by which the short form of ITI-H4 carries out its function remain obscure. Methods: Human sera and peripheral blood mononucleated cells (PBMCs) were collected from patients and normal controls to compare the expression levels of ITI-H4 and plasma kallikrein (KLKB1). Flow cytometric assay was performed to measure inflammatory markers in sera and culture supernatants. Furthermore, to investigate the functions of the two isoforms of ITI-H4, we performed migration, invasion, and proliferation assays. Findings: In the current study, we showed that ITI-H4 as a biomarker of RPL could be regulated by KLKB1 through the IL-6 signaling cascade, indicating a novel regulatory system for inflammation in RPL. In addition, our study indicates that the two isoforms of ITI-H4 possess opposing functions on immune response, trophoblast invasion, and monocytes migration or proliferation. Interpretation: The ITI-H4 (∆N688) might be a crucial inflammatory factor which contributes to the pathogenesis of RPL. Moreover, it is expected that this study would give some insights into potential functional mechanisms underlying RPL. Fund: This study was supported by the Ministry of Health & Welfare of the Republic of Korea (HI18C0378) through the Korea Health Industry Development Institute. Keywords: Early pregnancy loss, Immune tolerance, Migration and invasion, ITI-H4, Plasma kallikrein
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700	0		\|a Sang-Jin Song \|e verfasserin \|4 aut
700	0		\|a Chang-Zhu Pei \|e verfasserin \|4 aut
700	0		\|a Kwang Yul Lee \|e verfasserin \|4 aut
700	0		\|a Jinyoung Paek \|e verfasserin \|4 aut
700	0		\|a Kwang-Hyun Baek \|e verfasserin \|4 aut
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author_variant	l l ll b c c bcc j e r jer s j s sjs c z p czp k y l kyl j p jp k h b khb
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allfields	10.1016/j.ebiom.2018.10.029 doi (DE-627)DOAJ072299843 (DE-599)DOAJ69bd2e7ac2fd4889b0b7521c1750ffd5 DE-627 ger DE-627 rakwb eng R5-920 Lan Li verfasserin aut Opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy lossResearch in Context 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The mechanism behind an increased risk of recurrent pregnancy loss (RPL) remains largely unknown. In our previous study, we identified that inter-α-trypsin inhibitor heavy chain 4 (ITI-H4) is highly expressed at a modified molecular weight of 36 kDa in serum derived from RPL patients. Yet, the precise molecular mechanism and pathways by which the short form of ITI-H4 carries out its function remain obscure. Methods: Human sera and peripheral blood mononucleated cells (PBMCs) were collected from patients and normal controls to compare the expression levels of ITI-H4 and plasma kallikrein (KLKB1). Flow cytometric assay was performed to measure inflammatory markers in sera and culture supernatants. Furthermore, to investigate the functions of the two isoforms of ITI-H4, we performed migration, invasion, and proliferation assays. Findings: In the current study, we showed that ITI-H4 as a biomarker of RPL could be regulated by KLKB1 through the IL-6 signaling cascade, indicating a novel regulatory system for inflammation in RPL. In addition, our study indicates that the two isoforms of ITI-H4 possess opposing functions on immune response, trophoblast invasion, and monocytes migration or proliferation. Interpretation: The ITI-H4 (∆N688) might be a crucial inflammatory factor which contributes to the pathogenesis of RPL. Moreover, it is expected that this study would give some insights into potential functional mechanisms underlying RPL. Fund: This study was supported by the Ministry of Health & Welfare of the Republic of Korea (HI18C0378) through the Korea Health Industry Development Institute. Keywords: Early pregnancy loss, Immune tolerance, Migration and invasion, ITI-H4, Plasma kallikrein Medicine R Medicine (General) Bum-Chae Choi verfasserin aut Ji Eun Ryoo verfasserin aut Sang-Jin Song verfasserin aut Chang-Zhu Pei verfasserin aut Kwang Yul Lee verfasserin aut Jinyoung Paek verfasserin aut Kwang-Hyun Baek verfasserin aut In EBioMedicine Elsevier, 2015 37(2018), Seite 535-546 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:37 year:2018 pages:535-546 https://doi.org/10.1016/j.ebiom.2018.10.029 kostenfrei https://doaj.org/article/69bd2e7ac2fd4889b0b7521c1750ffd5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396418304493 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 37 2018 535-546
spelling	10.1016/j.ebiom.2018.10.029 doi (DE-627)DOAJ072299843 (DE-599)DOAJ69bd2e7ac2fd4889b0b7521c1750ffd5 DE-627 ger DE-627 rakwb eng R5-920 Lan Li verfasserin aut Opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy lossResearch in Context 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The mechanism behind an increased risk of recurrent pregnancy loss (RPL) remains largely unknown. In our previous study, we identified that inter-α-trypsin inhibitor heavy chain 4 (ITI-H4) is highly expressed at a modified molecular weight of 36 kDa in serum derived from RPL patients. Yet, the precise molecular mechanism and pathways by which the short form of ITI-H4 carries out its function remain obscure. Methods: Human sera and peripheral blood mononucleated cells (PBMCs) were collected from patients and normal controls to compare the expression levels of ITI-H4 and plasma kallikrein (KLKB1). Flow cytometric assay was performed to measure inflammatory markers in sera and culture supernatants. Furthermore, to investigate the functions of the two isoforms of ITI-H4, we performed migration, invasion, and proliferation assays. Findings: In the current study, we showed that ITI-H4 as a biomarker of RPL could be regulated by KLKB1 through the IL-6 signaling cascade, indicating a novel regulatory system for inflammation in RPL. In addition, our study indicates that the two isoforms of ITI-H4 possess opposing functions on immune response, trophoblast invasion, and monocytes migration or proliferation. Interpretation: The ITI-H4 (∆N688) might be a crucial inflammatory factor which contributes to the pathogenesis of RPL. Moreover, it is expected that this study would give some insights into potential functional mechanisms underlying RPL. Fund: This study was supported by the Ministry of Health & Welfare of the Republic of Korea (HI18C0378) through the Korea Health Industry Development Institute. Keywords: Early pregnancy loss, Immune tolerance, Migration and invasion, ITI-H4, Plasma kallikrein Medicine R Medicine (General) Bum-Chae Choi verfasserin aut Ji Eun Ryoo verfasserin aut Sang-Jin Song verfasserin aut Chang-Zhu Pei verfasserin aut Kwang Yul Lee verfasserin aut Jinyoung Paek verfasserin aut Kwang-Hyun Baek verfasserin aut In EBioMedicine Elsevier, 2015 37(2018), Seite 535-546 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:37 year:2018 pages:535-546 https://doi.org/10.1016/j.ebiom.2018.10.029 kostenfrei https://doaj.org/article/69bd2e7ac2fd4889b0b7521c1750ffd5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396418304493 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 37 2018 535-546
allfields_unstemmed	10.1016/j.ebiom.2018.10.029 doi (DE-627)DOAJ072299843 (DE-599)DOAJ69bd2e7ac2fd4889b0b7521c1750ffd5 DE-627 ger DE-627 rakwb eng R5-920 Lan Li verfasserin aut Opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy lossResearch in Context 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The mechanism behind an increased risk of recurrent pregnancy loss (RPL) remains largely unknown. In our previous study, we identified that inter-α-trypsin inhibitor heavy chain 4 (ITI-H4) is highly expressed at a modified molecular weight of 36 kDa in serum derived from RPL patients. Yet, the precise molecular mechanism and pathways by which the short form of ITI-H4 carries out its function remain obscure. Methods: Human sera and peripheral blood mononucleated cells (PBMCs) were collected from patients and normal controls to compare the expression levels of ITI-H4 and plasma kallikrein (KLKB1). Flow cytometric assay was performed to measure inflammatory markers in sera and culture supernatants. Furthermore, to investigate the functions of the two isoforms of ITI-H4, we performed migration, invasion, and proliferation assays. Findings: In the current study, we showed that ITI-H4 as a biomarker of RPL could be regulated by KLKB1 through the IL-6 signaling cascade, indicating a novel regulatory system for inflammation in RPL. In addition, our study indicates that the two isoforms of ITI-H4 possess opposing functions on immune response, trophoblast invasion, and monocytes migration or proliferation. Interpretation: The ITI-H4 (∆N688) might be a crucial inflammatory factor which contributes to the pathogenesis of RPL. Moreover, it is expected that this study would give some insights into potential functional mechanisms underlying RPL. Fund: This study was supported by the Ministry of Health & Welfare of the Republic of Korea (HI18C0378) through the Korea Health Industry Development Institute. Keywords: Early pregnancy loss, Immune tolerance, Migration and invasion, ITI-H4, Plasma kallikrein Medicine R Medicine (General) Bum-Chae Choi verfasserin aut Ji Eun Ryoo verfasserin aut Sang-Jin Song verfasserin aut Chang-Zhu Pei verfasserin aut Kwang Yul Lee verfasserin aut Jinyoung Paek verfasserin aut Kwang-Hyun Baek verfasserin aut In EBioMedicine Elsevier, 2015 37(2018), Seite 535-546 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:37 year:2018 pages:535-546 https://doi.org/10.1016/j.ebiom.2018.10.029 kostenfrei https://doaj.org/article/69bd2e7ac2fd4889b0b7521c1750ffd5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396418304493 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 37 2018 535-546
allfieldsGer	10.1016/j.ebiom.2018.10.029 doi (DE-627)DOAJ072299843 (DE-599)DOAJ69bd2e7ac2fd4889b0b7521c1750ffd5 DE-627 ger DE-627 rakwb eng R5-920 Lan Li verfasserin aut Opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy lossResearch in Context 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The mechanism behind an increased risk of recurrent pregnancy loss (RPL) remains largely unknown. In our previous study, we identified that inter-α-trypsin inhibitor heavy chain 4 (ITI-H4) is highly expressed at a modified molecular weight of 36 kDa in serum derived from RPL patients. Yet, the precise molecular mechanism and pathways by which the short form of ITI-H4 carries out its function remain obscure. Methods: Human sera and peripheral blood mononucleated cells (PBMCs) were collected from patients and normal controls to compare the expression levels of ITI-H4 and plasma kallikrein (KLKB1). Flow cytometric assay was performed to measure inflammatory markers in sera and culture supernatants. Furthermore, to investigate the functions of the two isoforms of ITI-H4, we performed migration, invasion, and proliferation assays. Findings: In the current study, we showed that ITI-H4 as a biomarker of RPL could be regulated by KLKB1 through the IL-6 signaling cascade, indicating a novel regulatory system for inflammation in RPL. In addition, our study indicates that the two isoforms of ITI-H4 possess opposing functions on immune response, trophoblast invasion, and monocytes migration or proliferation. Interpretation: The ITI-H4 (∆N688) might be a crucial inflammatory factor which contributes to the pathogenesis of RPL. Moreover, it is expected that this study would give some insights into potential functional mechanisms underlying RPL. Fund: This study was supported by the Ministry of Health & Welfare of the Republic of Korea (HI18C0378) through the Korea Health Industry Development Institute. Keywords: Early pregnancy loss, Immune tolerance, Migration and invasion, ITI-H4, Plasma kallikrein Medicine R Medicine (General) Bum-Chae Choi verfasserin aut Ji Eun Ryoo verfasserin aut Sang-Jin Song verfasserin aut Chang-Zhu Pei verfasserin aut Kwang Yul Lee verfasserin aut Jinyoung Paek verfasserin aut Kwang-Hyun Baek verfasserin aut In EBioMedicine Elsevier, 2015 37(2018), Seite 535-546 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:37 year:2018 pages:535-546 https://doi.org/10.1016/j.ebiom.2018.10.029 kostenfrei https://doaj.org/article/69bd2e7ac2fd4889b0b7521c1750ffd5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396418304493 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 37 2018 535-546
allfieldsSound	10.1016/j.ebiom.2018.10.029 doi (DE-627)DOAJ072299843 (DE-599)DOAJ69bd2e7ac2fd4889b0b7521c1750ffd5 DE-627 ger DE-627 rakwb eng R5-920 Lan Li verfasserin aut Opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy lossResearch in Context 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The mechanism behind an increased risk of recurrent pregnancy loss (RPL) remains largely unknown. In our previous study, we identified that inter-α-trypsin inhibitor heavy chain 4 (ITI-H4) is highly expressed at a modified molecular weight of 36 kDa in serum derived from RPL patients. Yet, the precise molecular mechanism and pathways by which the short form of ITI-H4 carries out its function remain obscure. Methods: Human sera and peripheral blood mononucleated cells (PBMCs) were collected from patients and normal controls to compare the expression levels of ITI-H4 and plasma kallikrein (KLKB1). Flow cytometric assay was performed to measure inflammatory markers in sera and culture supernatants. Furthermore, to investigate the functions of the two isoforms of ITI-H4, we performed migration, invasion, and proliferation assays. Findings: In the current study, we showed that ITI-H4 as a biomarker of RPL could be regulated by KLKB1 through the IL-6 signaling cascade, indicating a novel regulatory system for inflammation in RPL. In addition, our study indicates that the two isoforms of ITI-H4 possess opposing functions on immune response, trophoblast invasion, and monocytes migration or proliferation. Interpretation: The ITI-H4 (∆N688) might be a crucial inflammatory factor which contributes to the pathogenesis of RPL. Moreover, it is expected that this study would give some insights into potential functional mechanisms underlying RPL. Fund: This study was supported by the Ministry of Health & Welfare of the Republic of Korea (HI18C0378) through the Korea Health Industry Development Institute. Keywords: Early pregnancy loss, Immune tolerance, Migration and invasion, ITI-H4, Plasma kallikrein Medicine R Medicine (General) Bum-Chae Choi verfasserin aut Ji Eun Ryoo verfasserin aut Sang-Jin Song verfasserin aut Chang-Zhu Pei verfasserin aut Kwang Yul Lee verfasserin aut Jinyoung Paek verfasserin aut Kwang-Hyun Baek verfasserin aut In EBioMedicine Elsevier, 2015 37(2018), Seite 535-546 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:37 year:2018 pages:535-546 https://doi.org/10.1016/j.ebiom.2018.10.029 kostenfrei https://doaj.org/article/69bd2e7ac2fd4889b0b7521c1750ffd5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396418304493 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 37 2018 535-546
language	English
source	In EBioMedicine 37(2018), Seite 535-546 volume:37 year:2018 pages:535-546
sourceStr	In EBioMedicine 37(2018), Seite 535-546 volume:37 year:2018 pages:535-546
format_phy_str_mv	Article
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topic_facet	Medicine R Medicine (General)
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container_title	EBioMedicine
authorswithroles_txt_mv	Lan Li @@aut@@ Bum-Chae Choi @@aut@@ Ji Eun Ryoo @@aut@@ Sang-Jin Song @@aut@@ Chang-Zhu Pei @@aut@@ Kwang Yul Lee @@aut@@ Jinyoung Paek @@aut@@ Kwang-Hyun Baek @@aut@@
publishDateDaySort_date	2018-01-01T00:00:00Z
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In addition, our study indicates that the two isoforms of ITI-H4 possess opposing functions on immune response, trophoblast invasion, and monocytes migration or proliferation. Interpretation: The ITI-H4 (∆N688) might be a crucial inflammatory factor which contributes to the pathogenesis of RPL. Moreover, it is expected that this study would give some insights into potential functional mechanisms underlying RPL. Fund: This study was supported by the Ministry of Health & Welfare of the Republic of Korea (HI18C0378) through the Korea Health Industry Development Institute. 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callnumber-first	R - Medicine
author	Lan Li
spellingShingle	Lan Li misc R5-920 misc Medicine misc R misc Medicine (General) Opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy lossResearch in Context
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topic_title	R5-920 Opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy lossResearch in Context
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title	Opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy lossResearch in Context
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title_full	Opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy lossResearch in Context
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author_browse	Lan Li Bum-Chae Choi Ji Eun Ryoo Sang-Jin Song Chang-Zhu Pei Kwang Yul Lee Jinyoung Paek Kwang-Hyun Baek
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title_sort	opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy lossresearch in context
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title_auth	Opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy lossResearch in Context
abstract	Background: The mechanism behind an increased risk of recurrent pregnancy loss (RPL) remains largely unknown. In our previous study, we identified that inter-α-trypsin inhibitor heavy chain 4 (ITI-H4) is highly expressed at a modified molecular weight of 36 kDa in serum derived from RPL patients. Yet, the precise molecular mechanism and pathways by which the short form of ITI-H4 carries out its function remain obscure. Methods: Human sera and peripheral blood mononucleated cells (PBMCs) were collected from patients and normal controls to compare the expression levels of ITI-H4 and plasma kallikrein (KLKB1). Flow cytometric assay was performed to measure inflammatory markers in sera and culture supernatants. Furthermore, to investigate the functions of the two isoforms of ITI-H4, we performed migration, invasion, and proliferation assays. Findings: In the current study, we showed that ITI-H4 as a biomarker of RPL could be regulated by KLKB1 through the IL-6 signaling cascade, indicating a novel regulatory system for inflammation in RPL. In addition, our study indicates that the two isoforms of ITI-H4 possess opposing functions on immune response, trophoblast invasion, and monocytes migration or proliferation. Interpretation: The ITI-H4 (∆N688) might be a crucial inflammatory factor which contributes to the pathogenesis of RPL. Moreover, it is expected that this study would give some insights into potential functional mechanisms underlying RPL. Fund: This study was supported by the Ministry of Health & Welfare of the Republic of Korea (HI18C0378) through the Korea Health Industry Development Institute. Keywords: Early pregnancy loss, Immune tolerance, Migration and invasion, ITI-H4, Plasma kallikrein
abstractGer	Background: The mechanism behind an increased risk of recurrent pregnancy loss (RPL) remains largely unknown. In our previous study, we identified that inter-α-trypsin inhibitor heavy chain 4 (ITI-H4) is highly expressed at a modified molecular weight of 36 kDa in serum derived from RPL patients. Yet, the precise molecular mechanism and pathways by which the short form of ITI-H4 carries out its function remain obscure. Methods: Human sera and peripheral blood mononucleated cells (PBMCs) were collected from patients and normal controls to compare the expression levels of ITI-H4 and plasma kallikrein (KLKB1). Flow cytometric assay was performed to measure inflammatory markers in sera and culture supernatants. Furthermore, to investigate the functions of the two isoforms of ITI-H4, we performed migration, invasion, and proliferation assays. Findings: In the current study, we showed that ITI-H4 as a biomarker of RPL could be regulated by KLKB1 through the IL-6 signaling cascade, indicating a novel regulatory system for inflammation in RPL. In addition, our study indicates that the two isoforms of ITI-H4 possess opposing functions on immune response, trophoblast invasion, and monocytes migration or proliferation. Interpretation: The ITI-H4 (∆N688) might be a crucial inflammatory factor which contributes to the pathogenesis of RPL. Moreover, it is expected that this study would give some insights into potential functional mechanisms underlying RPL. Fund: This study was supported by the Ministry of Health & Welfare of the Republic of Korea (HI18C0378) through the Korea Health Industry Development Institute. Keywords: Early pregnancy loss, Immune tolerance, Migration and invasion, ITI-H4, Plasma kallikrein
abstract_unstemmed	Background: The mechanism behind an increased risk of recurrent pregnancy loss (RPL) remains largely unknown. In our previous study, we identified that inter-α-trypsin inhibitor heavy chain 4 (ITI-H4) is highly expressed at a modified molecular weight of 36 kDa in serum derived from RPL patients. Yet, the precise molecular mechanism and pathways by which the short form of ITI-H4 carries out its function remain obscure. Methods: Human sera and peripheral blood mononucleated cells (PBMCs) were collected from patients and normal controls to compare the expression levels of ITI-H4 and plasma kallikrein (KLKB1). Flow cytometric assay was performed to measure inflammatory markers in sera and culture supernatants. Furthermore, to investigate the functions of the two isoforms of ITI-H4, we performed migration, invasion, and proliferation assays. Findings: In the current study, we showed that ITI-H4 as a biomarker of RPL could be regulated by KLKB1 through the IL-6 signaling cascade, indicating a novel regulatory system for inflammation in RPL. In addition, our study indicates that the two isoforms of ITI-H4 possess opposing functions on immune response, trophoblast invasion, and monocytes migration or proliferation. Interpretation: The ITI-H4 (∆N688) might be a crucial inflammatory factor which contributes to the pathogenesis of RPL. Moreover, it is expected that this study would give some insights into potential functional mechanisms underlying RPL. Fund: This study was supported by the Ministry of Health & Welfare of the Republic of Korea (HI18C0378) through the Korea Health Industry Development Institute. Keywords: Early pregnancy loss, Immune tolerance, Migration and invasion, ITI-H4, Plasma kallikrein
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title_short	Opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy lossResearch in Context
url	https://doi.org/10.1016/j.ebiom.2018.10.029 https://doaj.org/article/69bd2e7ac2fd4889b0b7521c1750ffd5 http://www.sciencedirect.com/science/article/pii/S2352396418304493 https://doaj.org/toc/2352-3964
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In our previous study, we identified that inter-α-trypsin inhibitor heavy chain 4 (ITI-H4) is highly expressed at a modified molecular weight of 36 kDa in serum derived from RPL patients. Yet, the precise molecular mechanism and pathways by which the short form of ITI-H4 carries out its function remain obscure. Methods: Human sera and peripheral blood mononucleated cells (PBMCs) were collected from patients and normal controls to compare the expression levels of ITI-H4 and plasma kallikrein (KLKB1). Flow cytometric assay was performed to measure inflammatory markers in sera and culture supernatants. Furthermore, to investigate the functions of the two isoforms of ITI-H4, we performed migration, invasion, and proliferation assays. Findings: In the current study, we showed that ITI-H4 as a biomarker of RPL could be regulated by KLKB1 through the IL-6 signaling cascade, indicating a novel regulatory system for inflammation in RPL. In addition, our study indicates that the two isoforms of ITI-H4 possess opposing functions on immune response, trophoblast invasion, and monocytes migration or proliferation. Interpretation: The ITI-H4 (∆N688) might be a crucial inflammatory factor which contributes to the pathogenesis of RPL. Moreover, it is expected that this study would give some insights into potential functional mechanisms underlying RPL. Fund: This study was supported by the Ministry of Health & Welfare of the Republic of Korea (HI18C0378) through the Korea Health Industry Development Institute. 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Opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy lossResearch in Context

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