USP17 regulates preeclampsia by modulating the NF-κB signaling pathway via deubiquitinating HDAC2

Introduction: Ubiquitination is a significant post-translational modification engaged in diverse biological processes, such as cell differentiation, metastasis, and protein stability modulation. The dysregulation of ubiquitination and deubiquitination is inextricably linked to disease progression, i...
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Gespeichert in:

Autor*in:	Li, Aiping [verfasserIn] Wang, Ting [verfasserIn] Zhou, Shasha [verfasserIn] Han, Jingjing [verfasserIn] Wu, Wujia [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	Preeclampsia USP17 HDAC2 Deubiquitination NF-κB

Übergeordnetes Werk:	Enthalten in: Placenta - Amsterdam [u.a.] : Elsevier, 1980, 145, Seite 9-18
Übergeordnetes Werk:	volume:145 ; pages:9-18

DOI / URN:	10.1016/j.placenta.2023.11.010

Katalog-ID:	ELV066463343

Internformat


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035			\|a (DE-627)ELV066463343
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245	1	0	\|a USP17 regulates preeclampsia by modulating the NF-κB signaling pathway via deubiquitinating HDAC2
264		1	\|c 2023
336			\|a nicht spezifiziert \|b zzz \|2 rdacontent
337			\|a Computermedien \|b c \|2 rdamedia
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520			\|a Introduction: Ubiquitination is a significant post-translational modification engaged in diverse biological processes, such as cell differentiation, metastasis, and protein stability modulation. The dysregulation of ubiquitination and deubiquitination is inextricably linked to disease progression, including preeclampsia (PE). Ubiquitin-specific protease 17 (USP17), a prominent deubiquitinating enzyme that regulates ubiquitination modifications, performs multiple functions at the cellular level, whereas its role in PE remains elusive. In this study, we intended to probe the role of USP17 in PE and its underlying mechanisms.Methods: The USP17 level in the plasma of PE patients was detected through Elisa. Western blot and qRT-PCR were performed to measure the mRNA and protein level of USP17 in placental tissues. CCK-8, EdU, and transwell assays were conducted to evaluate the proliferation, migration, and invasion of trophoblast cells. The interaction between HDAC2 and USP17 or STAT1 were determined by co-immunoprecipitation and Western blot assays. The expression of NF-κB pathway related proteins was examined using Western blot.Results: USP17 was dramatically downregulated in PE patients. Overexpression of USP17 facilitated trophoblast proliferation, migration, and invasion. Moreover, histone deacetylase 2 (HDAC2) was validated as a substrate of USP17 deubiquitination, and USP17 upregulation enhanced HDAC2 protein level. Furthermore, HDAC2 could interact with and deacetylate Signal transducer and activator of transcription 1 (STAT1), resulting in the enhancement of STAT1 activity and inhibition of NF-κB signaling.Discussion: Our findings disclosed that USP17 augmented the proliferation and invasion of trophoblast by deubiquitinating HDAC2, which will contribute to novel prospective targets for diagnosing and treating PE.
650		4	\|a Preeclampsia
650		4	\|a USP17
650		4	\|a HDAC2
650		4	\|a Deubiquitination
650		4	\|a NF-κB
700	1		\|a Wang, Ting \|e verfasserin \|4 aut
700	1		\|a Zhou, Shasha \|e verfasserin \|4 aut
700	1		\|a Han, Jingjing \|e verfasserin \|4 aut
700	1		\|a Wu, Wujia \|e verfasserin \|4 aut
773	0	8	\|i Enthalten in \|t Placenta \|d Amsterdam [u.a.] : Elsevier, 1980 \|g 145, Seite 9-18 \|h Online-Ressource \|w (DE-627)320420442 \|w (DE-600)2002489-7 \|w (DE-576)106869582 \|x 1532-3102 \|7 nnns
773	1	8	\|g volume:145 \|g pages:9-18
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912			\|a GBV_ILN_2049
912			\|a GBV_ILN_2050
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912			\|a GBV_ILN_4323
912			\|a GBV_ILN_4324
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912			\|a GBV_ILN_4326
912			\|a GBV_ILN_4333
912			\|a GBV_ILN_4334
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4393
912			\|a GBV_ILN_4700
936	b	k	\|a 44.92 \|j Gynäkologie \|q VZ
951			\|a AR
952			\|d 145 \|h 9-18

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publishDate	2023
allfields	10.1016/j.placenta.2023.11.010 doi (DE-627)ELV066463343 (ELSEVIER)S0143-4004(23)00606-9 DE-627 ger DE-627 rda eng 610 VZ 44.92 bkl Li, Aiping verfasserin aut USP17 regulates preeclampsia by modulating the NF-κB signaling pathway via deubiquitinating HDAC2 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction: Ubiquitination is a significant post-translational modification engaged in diverse biological processes, such as cell differentiation, metastasis, and protein stability modulation. The dysregulation of ubiquitination and deubiquitination is inextricably linked to disease progression, including preeclampsia (PE). Ubiquitin-specific protease 17 (USP17), a prominent deubiquitinating enzyme that regulates ubiquitination modifications, performs multiple functions at the cellular level, whereas its role in PE remains elusive. In this study, we intended to probe the role of USP17 in PE and its underlying mechanisms.Methods: The USP17 level in the plasma of PE patients was detected through Elisa. Western blot and qRT-PCR were performed to measure the mRNA and protein level of USP17 in placental tissues. CCK-8, EdU, and transwell assays were conducted to evaluate the proliferation, migration, and invasion of trophoblast cells. The interaction between HDAC2 and USP17 or STAT1 were determined by co-immunoprecipitation and Western blot assays. The expression of NF-κB pathway related proteins was examined using Western blot.Results: USP17 was dramatically downregulated in PE patients. Overexpression of USP17 facilitated trophoblast proliferation, migration, and invasion. Moreover, histone deacetylase 2 (HDAC2) was validated as a substrate of USP17 deubiquitination, and USP17 upregulation enhanced HDAC2 protein level. Furthermore, HDAC2 could interact with and deacetylate Signal transducer and activator of transcription 1 (STAT1), resulting in the enhancement of STAT1 activity and inhibition of NF-κB signaling.Discussion: Our findings disclosed that USP17 augmented the proliferation and invasion of trophoblast by deubiquitinating HDAC2, which will contribute to novel prospective targets for diagnosing and treating PE. Preeclampsia USP17 HDAC2 Deubiquitination NF-κB Wang, Ting verfasserin aut Zhou, Shasha verfasserin aut Han, Jingjing verfasserin aut Wu, Wujia verfasserin aut Enthalten in Placenta Amsterdam [u.a.] : Elsevier, 1980 145, Seite 9-18 Online-Ressource (DE-627)320420442 (DE-600)2002489-7 (DE-576)106869582 1532-3102 nnns volume:145 pages:9-18 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.92 Gynäkologie VZ AR 145 9-18
spelling	10.1016/j.placenta.2023.11.010 doi (DE-627)ELV066463343 (ELSEVIER)S0143-4004(23)00606-9 DE-627 ger DE-627 rda eng 610 VZ 44.92 bkl Li, Aiping verfasserin aut USP17 regulates preeclampsia by modulating the NF-κB signaling pathway via deubiquitinating HDAC2 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction: Ubiquitination is a significant post-translational modification engaged in diverse biological processes, such as cell differentiation, metastasis, and protein stability modulation. The dysregulation of ubiquitination and deubiquitination is inextricably linked to disease progression, including preeclampsia (PE). Ubiquitin-specific protease 17 (USP17), a prominent deubiquitinating enzyme that regulates ubiquitination modifications, performs multiple functions at the cellular level, whereas its role in PE remains elusive. In this study, we intended to probe the role of USP17 in PE and its underlying mechanisms.Methods: The USP17 level in the plasma of PE patients was detected through Elisa. Western blot and qRT-PCR were performed to measure the mRNA and protein level of USP17 in placental tissues. CCK-8, EdU, and transwell assays were conducted to evaluate the proliferation, migration, and invasion of trophoblast cells. The interaction between HDAC2 and USP17 or STAT1 were determined by co-immunoprecipitation and Western blot assays. The expression of NF-κB pathway related proteins was examined using Western blot.Results: USP17 was dramatically downregulated in PE patients. Overexpression of USP17 facilitated trophoblast proliferation, migration, and invasion. Moreover, histone deacetylase 2 (HDAC2) was validated as a substrate of USP17 deubiquitination, and USP17 upregulation enhanced HDAC2 protein level. Furthermore, HDAC2 could interact with and deacetylate Signal transducer and activator of transcription 1 (STAT1), resulting in the enhancement of STAT1 activity and inhibition of NF-κB signaling.Discussion: Our findings disclosed that USP17 augmented the proliferation and invasion of trophoblast by deubiquitinating HDAC2, which will contribute to novel prospective targets for diagnosing and treating PE. Preeclampsia USP17 HDAC2 Deubiquitination NF-κB Wang, Ting verfasserin aut Zhou, Shasha verfasserin aut Han, Jingjing verfasserin aut Wu, Wujia verfasserin aut Enthalten in Placenta Amsterdam [u.a.] : Elsevier, 1980 145, Seite 9-18 Online-Ressource (DE-627)320420442 (DE-600)2002489-7 (DE-576)106869582 1532-3102 nnns volume:145 pages:9-18 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.92 Gynäkologie VZ AR 145 9-18
allfields_unstemmed	10.1016/j.placenta.2023.11.010 doi (DE-627)ELV066463343 (ELSEVIER)S0143-4004(23)00606-9 DE-627 ger DE-627 rda eng 610 VZ 44.92 bkl Li, Aiping verfasserin aut USP17 regulates preeclampsia by modulating the NF-κB signaling pathway via deubiquitinating HDAC2 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction: Ubiquitination is a significant post-translational modification engaged in diverse biological processes, such as cell differentiation, metastasis, and protein stability modulation. The dysregulation of ubiquitination and deubiquitination is inextricably linked to disease progression, including preeclampsia (PE). Ubiquitin-specific protease 17 (USP17), a prominent deubiquitinating enzyme that regulates ubiquitination modifications, performs multiple functions at the cellular level, whereas its role in PE remains elusive. In this study, we intended to probe the role of USP17 in PE and its underlying mechanisms.Methods: The USP17 level in the plasma of PE patients was detected through Elisa. Western blot and qRT-PCR were performed to measure the mRNA and protein level of USP17 in placental tissues. CCK-8, EdU, and transwell assays were conducted to evaluate the proliferation, migration, and invasion of trophoblast cells. The interaction between HDAC2 and USP17 or STAT1 were determined by co-immunoprecipitation and Western blot assays. The expression of NF-κB pathway related proteins was examined using Western blot.Results: USP17 was dramatically downregulated in PE patients. Overexpression of USP17 facilitated trophoblast proliferation, migration, and invasion. Moreover, histone deacetylase 2 (HDAC2) was validated as a substrate of USP17 deubiquitination, and USP17 upregulation enhanced HDAC2 protein level. Furthermore, HDAC2 could interact with and deacetylate Signal transducer and activator of transcription 1 (STAT1), resulting in the enhancement of STAT1 activity and inhibition of NF-κB signaling.Discussion: Our findings disclosed that USP17 augmented the proliferation and invasion of trophoblast by deubiquitinating HDAC2, which will contribute to novel prospective targets for diagnosing and treating PE. Preeclampsia USP17 HDAC2 Deubiquitination NF-κB Wang, Ting verfasserin aut Zhou, Shasha verfasserin aut Han, Jingjing verfasserin aut Wu, Wujia verfasserin aut Enthalten in Placenta Amsterdam [u.a.] : Elsevier, 1980 145, Seite 9-18 Online-Ressource (DE-627)320420442 (DE-600)2002489-7 (DE-576)106869582 1532-3102 nnns volume:145 pages:9-18 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.92 Gynäkologie VZ AR 145 9-18
allfieldsGer	10.1016/j.placenta.2023.11.010 doi (DE-627)ELV066463343 (ELSEVIER)S0143-4004(23)00606-9 DE-627 ger DE-627 rda eng 610 VZ 44.92 bkl Li, Aiping verfasserin aut USP17 regulates preeclampsia by modulating the NF-κB signaling pathway via deubiquitinating HDAC2 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction: Ubiquitination is a significant post-translational modification engaged in diverse biological processes, such as cell differentiation, metastasis, and protein stability modulation. The dysregulation of ubiquitination and deubiquitination is inextricably linked to disease progression, including preeclampsia (PE). Ubiquitin-specific protease 17 (USP17), a prominent deubiquitinating enzyme that regulates ubiquitination modifications, performs multiple functions at the cellular level, whereas its role in PE remains elusive. In this study, we intended to probe the role of USP17 in PE and its underlying mechanisms.Methods: The USP17 level in the plasma of PE patients was detected through Elisa. Western blot and qRT-PCR were performed to measure the mRNA and protein level of USP17 in placental tissues. CCK-8, EdU, and transwell assays were conducted to evaluate the proliferation, migration, and invasion of trophoblast cells. The interaction between HDAC2 and USP17 or STAT1 were determined by co-immunoprecipitation and Western blot assays. The expression of NF-κB pathway related proteins was examined using Western blot.Results: USP17 was dramatically downregulated in PE patients. Overexpression of USP17 facilitated trophoblast proliferation, migration, and invasion. Moreover, histone deacetylase 2 (HDAC2) was validated as a substrate of USP17 deubiquitination, and USP17 upregulation enhanced HDAC2 protein level. Furthermore, HDAC2 could interact with and deacetylate Signal transducer and activator of transcription 1 (STAT1), resulting in the enhancement of STAT1 activity and inhibition of NF-κB signaling.Discussion: Our findings disclosed that USP17 augmented the proliferation and invasion of trophoblast by deubiquitinating HDAC2, which will contribute to novel prospective targets for diagnosing and treating PE. Preeclampsia USP17 HDAC2 Deubiquitination NF-κB Wang, Ting verfasserin aut Zhou, Shasha verfasserin aut Han, Jingjing verfasserin aut Wu, Wujia verfasserin aut Enthalten in Placenta Amsterdam [u.a.] : Elsevier, 1980 145, Seite 9-18 Online-Ressource (DE-627)320420442 (DE-600)2002489-7 (DE-576)106869582 1532-3102 nnns volume:145 pages:9-18 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.92 Gynäkologie VZ AR 145 9-18
allfieldsSound	10.1016/j.placenta.2023.11.010 doi (DE-627)ELV066463343 (ELSEVIER)S0143-4004(23)00606-9 DE-627 ger DE-627 rda eng 610 VZ 44.92 bkl Li, Aiping verfasserin aut USP17 regulates preeclampsia by modulating the NF-κB signaling pathway via deubiquitinating HDAC2 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction: Ubiquitination is a significant post-translational modification engaged in diverse biological processes, such as cell differentiation, metastasis, and protein stability modulation. The dysregulation of ubiquitination and deubiquitination is inextricably linked to disease progression, including preeclampsia (PE). Ubiquitin-specific protease 17 (USP17), a prominent deubiquitinating enzyme that regulates ubiquitination modifications, performs multiple functions at the cellular level, whereas its role in PE remains elusive. In this study, we intended to probe the role of USP17 in PE and its underlying mechanisms.Methods: The USP17 level in the plasma of PE patients was detected through Elisa. Western blot and qRT-PCR were performed to measure the mRNA and protein level of USP17 in placental tissues. CCK-8, EdU, and transwell assays were conducted to evaluate the proliferation, migration, and invasion of trophoblast cells. The interaction between HDAC2 and USP17 or STAT1 were determined by co-immunoprecipitation and Western blot assays. The expression of NF-κB pathway related proteins was examined using Western blot.Results: USP17 was dramatically downregulated in PE patients. Overexpression of USP17 facilitated trophoblast proliferation, migration, and invasion. Moreover, histone deacetylase 2 (HDAC2) was validated as a substrate of USP17 deubiquitination, and USP17 upregulation enhanced HDAC2 protein level. Furthermore, HDAC2 could interact with and deacetylate Signal transducer and activator of transcription 1 (STAT1), resulting in the enhancement of STAT1 activity and inhibition of NF-κB signaling.Discussion: Our findings disclosed that USP17 augmented the proliferation and invasion of trophoblast by deubiquitinating HDAC2, which will contribute to novel prospective targets for diagnosing and treating PE. Preeclampsia USP17 HDAC2 Deubiquitination NF-κB Wang, Ting verfasserin aut Zhou, Shasha verfasserin aut Han, Jingjing verfasserin aut Wu, Wujia verfasserin aut Enthalten in Placenta Amsterdam [u.a.] : Elsevier, 1980 145, Seite 9-18 Online-Ressource (DE-627)320420442 (DE-600)2002489-7 (DE-576)106869582 1532-3102 nnns volume:145 pages:9-18 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.92 Gynäkologie VZ AR 145 9-18
language	English
source	Enthalten in Placenta 145, Seite 9-18 volume:145 pages:9-18
sourceStr	Enthalten in Placenta 145, Seite 9-18 volume:145 pages:9-18
format_phy_str_mv	Article
bklname	Gynäkologie
institution	findex.gbv.de
topic_facet	Preeclampsia USP17 HDAC2 Deubiquitination NF-κB
dewey-raw	610
isfreeaccess_bool	false
container_title	Placenta
authorswithroles_txt_mv	Li, Aiping @@aut@@ Wang, Ting @@aut@@ Zhou, Shasha @@aut@@ Han, Jingjing @@aut@@ Wu, Wujia @@aut@@
publishDateDaySort_date	2023-01-01T00:00:00Z
hierarchy_top_id	320420442
dewey-sort	3610
id	ELV066463343
language_de	englisch
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The expression of NF-κB pathway related proteins was examined using Western blot.Results: USP17 was dramatically downregulated in PE patients. Overexpression of USP17 facilitated trophoblast proliferation, migration, and invasion. Moreover, histone deacetylase 2 (HDAC2) was validated as a substrate of USP17 deubiquitination, and USP17 upregulation enhanced HDAC2 protein level. 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author	Li, Aiping
spellingShingle	Li, Aiping ddc 610 bkl 44.92 misc Preeclampsia misc USP17 misc HDAC2 misc Deubiquitination misc NF-κB USP17 regulates preeclampsia by modulating the NF-κB signaling pathway via deubiquitinating HDAC2
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topic_title	610 VZ 44.92 bkl USP17 regulates preeclampsia by modulating the NF-κB signaling pathway via deubiquitinating HDAC2 Preeclampsia USP17 HDAC2 Deubiquitination NF-κB
topic	ddc 610 bkl 44.92 misc Preeclampsia misc USP17 misc HDAC2 misc Deubiquitination misc NF-κB
topic_unstemmed	ddc 610 bkl 44.92 misc Preeclampsia misc USP17 misc HDAC2 misc Deubiquitination misc NF-κB
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title	USP17 regulates preeclampsia by modulating the NF-κB signaling pathway via deubiquitinating HDAC2
ctrlnum	(DE-627)ELV066463343 (ELSEVIER)S0143-4004(23)00606-9
title_full	USP17 regulates preeclampsia by modulating the NF-κB signaling pathway via deubiquitinating HDAC2
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journal	Placenta
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dewey-full	610
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title_sort	usp17 regulates preeclampsia by modulating the nf-κb signaling pathway via deubiquitinating hdac2
title_auth	USP17 regulates preeclampsia by modulating the NF-κB signaling pathway via deubiquitinating HDAC2
abstract	Introduction: Ubiquitination is a significant post-translational modification engaged in diverse biological processes, such as cell differentiation, metastasis, and protein stability modulation. The dysregulation of ubiquitination and deubiquitination is inextricably linked to disease progression, including preeclampsia (PE). Ubiquitin-specific protease 17 (USP17), a prominent deubiquitinating enzyme that regulates ubiquitination modifications, performs multiple functions at the cellular level, whereas its role in PE remains elusive. In this study, we intended to probe the role of USP17 in PE and its underlying mechanisms.Methods: The USP17 level in the plasma of PE patients was detected through Elisa. Western blot and qRT-PCR were performed to measure the mRNA and protein level of USP17 in placental tissues. CCK-8, EdU, and transwell assays were conducted to evaluate the proliferation, migration, and invasion of trophoblast cells. The interaction between HDAC2 and USP17 or STAT1 were determined by co-immunoprecipitation and Western blot assays. The expression of NF-κB pathway related proteins was examined using Western blot.Results: USP17 was dramatically downregulated in PE patients. Overexpression of USP17 facilitated trophoblast proliferation, migration, and invasion. Moreover, histone deacetylase 2 (HDAC2) was validated as a substrate of USP17 deubiquitination, and USP17 upregulation enhanced HDAC2 protein level. Furthermore, HDAC2 could interact with and deacetylate Signal transducer and activator of transcription 1 (STAT1), resulting in the enhancement of STAT1 activity and inhibition of NF-κB signaling.Discussion: Our findings disclosed that USP17 augmented the proliferation and invasion of trophoblast by deubiquitinating HDAC2, which will contribute to novel prospective targets for diagnosing and treating PE.
abstractGer	Introduction: Ubiquitination is a significant post-translational modification engaged in diverse biological processes, such as cell differentiation, metastasis, and protein stability modulation. The dysregulation of ubiquitination and deubiquitination is inextricably linked to disease progression, including preeclampsia (PE). Ubiquitin-specific protease 17 (USP17), a prominent deubiquitinating enzyme that regulates ubiquitination modifications, performs multiple functions at the cellular level, whereas its role in PE remains elusive. In this study, we intended to probe the role of USP17 in PE and its underlying mechanisms.Methods: The USP17 level in the plasma of PE patients was detected through Elisa. Western blot and qRT-PCR were performed to measure the mRNA and protein level of USP17 in placental tissues. CCK-8, EdU, and transwell assays were conducted to evaluate the proliferation, migration, and invasion of trophoblast cells. The interaction between HDAC2 and USP17 or STAT1 were determined by co-immunoprecipitation and Western blot assays. The expression of NF-κB pathway related proteins was examined using Western blot.Results: USP17 was dramatically downregulated in PE patients. Overexpression of USP17 facilitated trophoblast proliferation, migration, and invasion. Moreover, histone deacetylase 2 (HDAC2) was validated as a substrate of USP17 deubiquitination, and USP17 upregulation enhanced HDAC2 protein level. Furthermore, HDAC2 could interact with and deacetylate Signal transducer and activator of transcription 1 (STAT1), resulting in the enhancement of STAT1 activity and inhibition of NF-κB signaling.Discussion: Our findings disclosed that USP17 augmented the proliferation and invasion of trophoblast by deubiquitinating HDAC2, which will contribute to novel prospective targets for diagnosing and treating PE.
abstract_unstemmed	Introduction: Ubiquitination is a significant post-translational modification engaged in diverse biological processes, such as cell differentiation, metastasis, and protein stability modulation. The dysregulation of ubiquitination and deubiquitination is inextricably linked to disease progression, including preeclampsia (PE). Ubiquitin-specific protease 17 (USP17), a prominent deubiquitinating enzyme that regulates ubiquitination modifications, performs multiple functions at the cellular level, whereas its role in PE remains elusive. In this study, we intended to probe the role of USP17 in PE and its underlying mechanisms.Methods: The USP17 level in the plasma of PE patients was detected through Elisa. Western blot and qRT-PCR were performed to measure the mRNA and protein level of USP17 in placental tissues. CCK-8, EdU, and transwell assays were conducted to evaluate the proliferation, migration, and invasion of trophoblast cells. The interaction between HDAC2 and USP17 or STAT1 were determined by co-immunoprecipitation and Western blot assays. The expression of NF-κB pathway related proteins was examined using Western blot.Results: USP17 was dramatically downregulated in PE patients. Overexpression of USP17 facilitated trophoblast proliferation, migration, and invasion. Moreover, histone deacetylase 2 (HDAC2) was validated as a substrate of USP17 deubiquitination, and USP17 upregulation enhanced HDAC2 protein level. Furthermore, HDAC2 could interact with and deacetylate Signal transducer and activator of transcription 1 (STAT1), resulting in the enhancement of STAT1 activity and inhibition of NF-κB signaling.Discussion: Our findings disclosed that USP17 augmented the proliferation and invasion of trophoblast by deubiquitinating HDAC2, which will contribute to novel prospective targets for diagnosing and treating PE.
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title_short	USP17 regulates preeclampsia by modulating the NF-κB signaling pathway via deubiquitinating HDAC2
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author2	Wang, Ting Zhou, Shasha Han, Jingjing Wu, Wujia
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doi_str	10.1016/j.placenta.2023.11.010
up_date	2024-07-06T17:50:53.568Z
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