Electroacupuncture Attenuated Phenotype Transformation of Vascular Smooth Muscle Cells via PI3K/Akt and MAPK Signaling Pathways in Spontaneous Hypertensive Rats
Objective To investigate whether the antihypertensive mechanism of electroacupuncture (EA) is associated with attenuating phenotype transformation of vascular smooth muscle cells (VSMCs) via phosphoinositide3-kinase (PI3K)/protein kinase B (Akt) and mitogen-activated protein kinase (MAPK) signaling...
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| Veröffentlicht in: | Chinese journal of integrative medicine 2022-04, Vol.28 (4), p.357-365 |
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| creator | Chen, Xin-yu Yang, Lu-ping Zheng, Ya-ling Li, Yu-xi Zhong, Dong-ling Jin, Rong-jiang Li, Juan |
| description | Objective
To investigate whether the antihypertensive mechanism of electroacupuncture (EA) is associated with attenuating phenotype transformation of vascular smooth muscle cells (VSMCs) via phosphoinositide3-kinase (PI3K)/protein kinase B (Akt) and mitogen-activated protein kinase (MAPK) signaling pathways.
Methods
Eight Wistar-ktoyo (WKY) rats were set as normal blood pressure group (normal group). A total of 32 spontaneous hypertensive rats (SHRs) were randomly divided into 4 groups using random number tables: a model group, an EA group, an EA+PI3K antagonist group (EA+P group), and an EA+p38 MAPK agonist+extracellular signal-regulated kinase (ERK) agonist group (EA+M group) (
n
=8/group). SHRs in EA group, EA+P group and EA+M group received EA treatment 5 sessions per week for continuous 4 weeks, while rats in the normal and model groups were bundled in same condition. The systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) of each rat was measured at 0 week and the 4th week. After 4-week intervention, thoracic aorta was collected for hematoxylin-eosin (HE) staining, immunohistochemistry [the contractile markers α-smooth muscle actin (α-SMA) and calponin and the synthetic marker osteopontin (OPN)] and Western blot [α-SMA, calponin, OPN, PI3K, phosphorylated-Akt (p-Akt), Akt, p-p42/44 ERK, total p42/44 ERK, p-p38 MAPK and total p38 MAPK].
Results
EA significantly reduced SBP, DBP and MAP (
P |
| doi_str_mv | 10.1007/s11655-021-2883-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2604455894</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2604455894</sourcerecordid><originalsourceid>FETCH-LOGICAL-c344t-9729a6d83820cf8c2831ed8fe784167cf360ca444019635b1ebb4c218c6e378f3</originalsourceid><addsrcrecordid>eNp9kc1u1DAUhS1ERUvLA7BBXrIJ9V8SZzkatbRqK0adlq3lcW5mUhI7-Kcob8Oj4iqFJat7pXvuufb5EPpIyRdKSH0eKK3KsiCMFkxKXsxv0AltGl4QQdjb3Fc1yz0tj9H7EJ4IKeuKlO_QMReSN6IsT9DviwFM9E6bNCVrYvKAVzGCTTpCizcHsC7OE-AHr23onB917J3FrsPfdTBp0B5vR-fiAd-lYAbAaxiGgJ97jTfX_OZ89SNibVt8t9rc4G2_t3ro7R5vdDz80nPAvcXbydmoLbgU8FW-5fP50D8DvtcxnKGjTg8BPrzWU_R4efGwvipuv329Xq9uC8OFiEVTs0ZXreSSEdNJwySn0MoOailyDKbjFTFaCEFoU_FyR2G3E4ZRaSrgtez4Kfq8-E7e_UwQohr7YPJflocpVhGRE5ONyFK6SI13IXjo1OT7UftZUaJewKgFjMpg1AsYNeedT6_2aTdC-2_jL4ksYIsg5JHdg1dPLvmcVviP6x-e95vt</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2604455894</pqid></control><display><type>article</type><title>Electroacupuncture Attenuated Phenotype Transformation of Vascular Smooth Muscle Cells via PI3K/Akt and MAPK Signaling Pathways in Spontaneous Hypertensive Rats</title><source>MEDLINE</source><source>Alma/SFX Local Collection</source><source>SpringerLink Journals - AutoHoldings</source><creator>Chen, Xin-yu ; Yang, Lu-ping ; Zheng, Ya-ling ; Li, Yu-xi ; Zhong, Dong-ling ; Jin, Rong-jiang ; Li, Juan</creator><creatorcontrib>Chen, Xin-yu ; Yang, Lu-ping ; Zheng, Ya-ling ; Li, Yu-xi ; Zhong, Dong-ling ; Jin, Rong-jiang ; Li, Juan</creatorcontrib><description>Objective
To investigate whether the antihypertensive mechanism of electroacupuncture (EA) is associated with attenuating phenotype transformation of vascular smooth muscle cells (VSMCs) via phosphoinositide3-kinase (PI3K)/protein kinase B (Akt) and mitogen-activated protein kinase (MAPK) signaling pathways.
Methods
Eight Wistar-ktoyo (WKY) rats were set as normal blood pressure group (normal group). A total of 32 spontaneous hypertensive rats (SHRs) were randomly divided into 4 groups using random number tables: a model group, an EA group, an EA+PI3K antagonist group (EA+P group), and an EA+p38 MAPK agonist+extracellular signal-regulated kinase (ERK) agonist group (EA+M group) (
n
=8/group). SHRs in EA group, EA+P group and EA+M group received EA treatment 5 sessions per week for continuous 4 weeks, while rats in the normal and model groups were bundled in same condition. The systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) of each rat was measured at 0 week and the 4th week. After 4-week intervention, thoracic aorta was collected for hematoxylin-eosin (HE) staining, immunohistochemistry [the contractile markers α-smooth muscle actin (α-SMA) and calponin and the synthetic marker osteopontin (OPN)] and Western blot [α-SMA, calponin, OPN, PI3K, phosphorylated-Akt (p-Akt), Akt, p-p42/44 ERK, total p42/44 ERK, p-p38 MAPK and total p38 MAPK].
Results
EA significantly reduced SBP, DBP and MAP (
P
<0.01). HE staining showed that the wall thickness of thoracic aorta in EA group was significantly decreased (
P
<0.01). From results of immunohistochemistry and Western blot, EA increased the expression of α-SMA and calponin, and decreased the expression of OPN (
P
<0.01). In addition, the expression of PI3K and p-Akt increased (
P
<0.01), while the expression of p-p42/44 ERK and p-p38 MAPK decreased in EA group (
P
<0.01). However, these effects were reversed by PI3K antagonist, p38 MAPK agonist and ERK agonist.
Conclusions
EA was an effective treatment for BP management. The antihypertensive effect of EA may be related with inhibition of phenotypic transformation of VSMCs, in which the activation of PI3K/Akt and the repression of MAPK pathway were involved.</description><identifier>ISSN: 1672-0415</identifier><identifier>EISSN: 1993-0402</identifier><identifier>DOI: 10.1007/s11655-021-2883-y</identifier><identifier>PMID: 34839455</identifier><language>eng</language><publisher>Singapore: Springer Singapore</publisher><subject>Acupuncture Research ; Animals ; Electroacupuncture ; Extracellular Signal-Regulated MAP Kinases - metabolism ; MAP Kinase Signaling System ; Medicine ; Medicine & Public Health ; Muscle, Smooth, Vascular ; Phenotype ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Inbred SHR</subject><ispartof>Chinese journal of integrative medicine, 2022-04, Vol.28 (4), p.357-365</ispartof><rights>The Chinese Journal of Integrated Traditional and Western Medicine Press and Springer-Verlag GmbH Germany, part of Springer Nature 2021</rights><rights>2021. The Chinese Journal of Integrated Traditional and Western Medicine Press and Springer-Verlag GmbH Germany, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c344t-9729a6d83820cf8c2831ed8fe784167cf360ca444019635b1ebb4c218c6e378f3</citedby><cites>FETCH-LOGICAL-c344t-9729a6d83820cf8c2831ed8fe784167cf360ca444019635b1ebb4c218c6e378f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11655-021-2883-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11655-021-2883-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34839455$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Xin-yu</creatorcontrib><creatorcontrib>Yang, Lu-ping</creatorcontrib><creatorcontrib>Zheng, Ya-ling</creatorcontrib><creatorcontrib>Li, Yu-xi</creatorcontrib><creatorcontrib>Zhong, Dong-ling</creatorcontrib><creatorcontrib>Jin, Rong-jiang</creatorcontrib><creatorcontrib>Li, Juan</creatorcontrib><title>Electroacupuncture Attenuated Phenotype Transformation of Vascular Smooth Muscle Cells via PI3K/Akt and MAPK Signaling Pathways in Spontaneous Hypertensive Rats</title><title>Chinese journal of integrative medicine</title><addtitle>Chin. J. Integr. Med</addtitle><addtitle>Chin J Integr Med</addtitle><description>Objective
To investigate whether the antihypertensive mechanism of electroacupuncture (EA) is associated with attenuating phenotype transformation of vascular smooth muscle cells (VSMCs) via phosphoinositide3-kinase (PI3K)/protein kinase B (Akt) and mitogen-activated protein kinase (MAPK) signaling pathways.
Methods
Eight Wistar-ktoyo (WKY) rats were set as normal blood pressure group (normal group). A total of 32 spontaneous hypertensive rats (SHRs) were randomly divided into 4 groups using random number tables: a model group, an EA group, an EA+PI3K antagonist group (EA+P group), and an EA+p38 MAPK agonist+extracellular signal-regulated kinase (ERK) agonist group (EA+M group) (
n
=8/group). SHRs in EA group, EA+P group and EA+M group received EA treatment 5 sessions per week for continuous 4 weeks, while rats in the normal and model groups were bundled in same condition. The systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) of each rat was measured at 0 week and the 4th week. After 4-week intervention, thoracic aorta was collected for hematoxylin-eosin (HE) staining, immunohistochemistry [the contractile markers α-smooth muscle actin (α-SMA) and calponin and the synthetic marker osteopontin (OPN)] and Western blot [α-SMA, calponin, OPN, PI3K, phosphorylated-Akt (p-Akt), Akt, p-p42/44 ERK, total p42/44 ERK, p-p38 MAPK and total p38 MAPK].
Results
EA significantly reduced SBP, DBP and MAP (
P
<0.01). HE staining showed that the wall thickness of thoracic aorta in EA group was significantly decreased (
P
<0.01). From results of immunohistochemistry and Western blot, EA increased the expression of α-SMA and calponin, and decreased the expression of OPN (
P
<0.01). In addition, the expression of PI3K and p-Akt increased (
P
<0.01), while the expression of p-p42/44 ERK and p-p38 MAPK decreased in EA group (
P
<0.01). However, these effects were reversed by PI3K antagonist, p38 MAPK agonist and ERK agonist.
Conclusions
EA was an effective treatment for BP management. The antihypertensive effect of EA may be related with inhibition of phenotypic transformation of VSMCs, in which the activation of PI3K/Akt and the repression of MAPK pathway were involved.</description><subject>Acupuncture Research</subject><subject>Animals</subject><subject>Electroacupuncture</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>MAP Kinase Signaling System</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Muscle, Smooth, Vascular</subject><subject>Phenotype</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><issn>1672-0415</issn><issn>1993-0402</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1u1DAUhS1ERUvLA7BBXrIJ9V8SZzkatbRqK0adlq3lcW5mUhI7-Kcob8Oj4iqFJat7pXvuufb5EPpIyRdKSH0eKK3KsiCMFkxKXsxv0AltGl4QQdjb3Fc1yz0tj9H7EJ4IKeuKlO_QMReSN6IsT9DviwFM9E6bNCVrYvKAVzGCTTpCizcHsC7OE-AHr23onB917J3FrsPfdTBp0B5vR-fiAd-lYAbAaxiGgJ97jTfX_OZ89SNibVt8t9rc4G2_t3ro7R5vdDz80nPAvcXbydmoLbgU8FW-5fP50D8DvtcxnKGjTg8BPrzWU_R4efGwvipuv329Xq9uC8OFiEVTs0ZXreSSEdNJwySn0MoOailyDKbjFTFaCEFoU_FyR2G3E4ZRaSrgtez4Kfq8-E7e_UwQohr7YPJflocpVhGRE5ONyFK6SI13IXjo1OT7UftZUaJewKgFjMpg1AsYNeedT6_2aTdC-2_jL4ksYIsg5JHdg1dPLvmcVviP6x-e95vt</recordid><startdate>20220401</startdate><enddate>20220401</enddate><creator>Chen, Xin-yu</creator><creator>Yang, Lu-ping</creator><creator>Zheng, Ya-ling</creator><creator>Li, Yu-xi</creator><creator>Zhong, Dong-ling</creator><creator>Jin, Rong-jiang</creator><creator>Li, Juan</creator><general>Springer Singapore</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20220401</creationdate><title>Electroacupuncture Attenuated Phenotype Transformation of Vascular Smooth Muscle Cells via PI3K/Akt and MAPK Signaling Pathways in Spontaneous Hypertensive Rats</title><author>Chen, Xin-yu ; Yang, Lu-ping ; Zheng, Ya-ling ; Li, Yu-xi ; Zhong, Dong-ling ; Jin, Rong-jiang ; Li, Juan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c344t-9729a6d83820cf8c2831ed8fe784167cf360ca444019635b1ebb4c218c6e378f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Acupuncture Research</topic><topic>Animals</topic><topic>Electroacupuncture</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>MAP Kinase Signaling System</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Muscle, Smooth, Vascular</topic><topic>Phenotype</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Xin-yu</creatorcontrib><creatorcontrib>Yang, Lu-ping</creatorcontrib><creatorcontrib>Zheng, Ya-ling</creatorcontrib><creatorcontrib>Li, Yu-xi</creatorcontrib><creatorcontrib>Zhong, Dong-ling</creatorcontrib><creatorcontrib>Jin, Rong-jiang</creatorcontrib><creatorcontrib>Li, Juan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Chinese journal of integrative medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Xin-yu</au><au>Yang, Lu-ping</au><au>Zheng, Ya-ling</au><au>Li, Yu-xi</au><au>Zhong, Dong-ling</au><au>Jin, Rong-jiang</au><au>Li, Juan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Electroacupuncture Attenuated Phenotype Transformation of Vascular Smooth Muscle Cells via PI3K/Akt and MAPK Signaling Pathways in Spontaneous Hypertensive Rats</atitle><jtitle>Chinese journal of integrative medicine</jtitle><stitle>Chin. J. Integr. Med</stitle><addtitle>Chin J Integr Med</addtitle><date>2022-04-01</date><risdate>2022</risdate><volume>28</volume><issue>4</issue><spage>357</spage><epage>365</epage><pages>357-365</pages><issn>1672-0415</issn><eissn>1993-0402</eissn><abstract>Objective
To investigate whether the antihypertensive mechanism of electroacupuncture (EA) is associated with attenuating phenotype transformation of vascular smooth muscle cells (VSMCs) via phosphoinositide3-kinase (PI3K)/protein kinase B (Akt) and mitogen-activated protein kinase (MAPK) signaling pathways.
Methods
Eight Wistar-ktoyo (WKY) rats were set as normal blood pressure group (normal group). A total of 32 spontaneous hypertensive rats (SHRs) were randomly divided into 4 groups using random number tables: a model group, an EA group, an EA+PI3K antagonist group (EA+P group), and an EA+p38 MAPK agonist+extracellular signal-regulated kinase (ERK) agonist group (EA+M group) (
n
=8/group). SHRs in EA group, EA+P group and EA+M group received EA treatment 5 sessions per week for continuous 4 weeks, while rats in the normal and model groups were bundled in same condition. The systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) of each rat was measured at 0 week and the 4th week. After 4-week intervention, thoracic aorta was collected for hematoxylin-eosin (HE) staining, immunohistochemistry [the contractile markers α-smooth muscle actin (α-SMA) and calponin and the synthetic marker osteopontin (OPN)] and Western blot [α-SMA, calponin, OPN, PI3K, phosphorylated-Akt (p-Akt), Akt, p-p42/44 ERK, total p42/44 ERK, p-p38 MAPK and total p38 MAPK].
Results
EA significantly reduced SBP, DBP and MAP (
P
<0.01). HE staining showed that the wall thickness of thoracic aorta in EA group was significantly decreased (
P
<0.01). From results of immunohistochemistry and Western blot, EA increased the expression of α-SMA and calponin, and decreased the expression of OPN (
P
<0.01). In addition, the expression of PI3K and p-Akt increased (
P
<0.01), while the expression of p-p42/44 ERK and p-p38 MAPK decreased in EA group (
P
<0.01). However, these effects were reversed by PI3K antagonist, p38 MAPK agonist and ERK agonist.
Conclusions
EA was an effective treatment for BP management. The antihypertensive effect of EA may be related with inhibition of phenotypic transformation of VSMCs, in which the activation of PI3K/Akt and the repression of MAPK pathway were involved.</abstract><cop>Singapore</cop><pub>Springer Singapore</pub><pmid>34839455</pmid><doi>10.1007/s11655-021-2883-y</doi><tpages>9</tpages></addata></record> |
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| ispartof | Chinese journal of integrative medicine, 2022-04, Vol.28 (4), p.357-365 |
| issn | 1672-0415 1993-0402 |
| language | eng |
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| source | MEDLINE; Alma/SFX Local Collection; SpringerLink Journals - AutoHoldings |
| subjects | Acupuncture Research Animals Electroacupuncture Extracellular Signal-Regulated MAP Kinases - metabolism MAP Kinase Signaling System Medicine Medicine & Public Health Muscle, Smooth, Vascular Phenotype Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Inbred SHR |
| title | Electroacupuncture Attenuated Phenotype Transformation of Vascular Smooth Muscle Cells via PI3K/Akt and MAPK Signaling Pathways in Spontaneous Hypertensive Rats |
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