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Substance P activates both contractile and inflammatory pathways in lymphatics through the neurokinin receptors NK1R and NK3R

Identifieur interne : 002931 ( Pmc/Curation ); précédent : 002930; suivant : 002932

Substance P activates both contractile and inflammatory pathways in lymphatics through the neurokinin receptors NK1R and NK3R

Auteurs : Sanjukta Chakraborty [États-Unis] ; Zhanna Nepiyushchikh [États-Unis] ; Michael J. Davis [États-Unis] ; David C. Zawieja [États-Unis] ; Mariappan Muthuchamy [États-Unis]

Source :

Microcirculation (New York, N.Y. : 1994) [ 1073-9688 ] ; 2011.

RBID : PMC:3058475

Abstract

Objective

The aim of this study was to elucidate the molecular signaling mechanisms by which substance P (SP) modulates lymphatic muscle contraction and to determine whether SP stimulates both contractile as well as inflammatory pathways in the lymphatics.

Methods

A rat mesenteric lymphatic muscle cell culture model (RMLMCs) and known specific pharmacological inhibitors were utilized to delineate SP mediated signaling pathways in lymphatics.

Results

We detected expression of neurokinin receptor 1 (NK1R) and neurokinin receptor 3 (NK3R) in RMLMCs. SP stimulation increased phosphorylation of myosin light chain 20 (MLC₂₀) as well as p38 mitogen associated protein kinase (p38-MAPK) and extracellular signal regulated kinase (ERK1/2) indicating activation of both a contractile and a pro-inflammatory MAPK pathway. Pharmacological inhibition of both NK1R and NK3R significantly affected the downstream SP signaling. We further examined whether there was any crosstalk between the two pathways upon SP stimulation. Inhibition of ERK1/2 decreased levels of p-MLC₂₀ after SP activation, in a PKC dependent manner, indicating a potential crosstalk between these two pathways.

Conclusions

These data provide the first evidence that SP mediated crosstalk between pro-inflammatory and contractile signaling mechanisms exists in the lymphatic system and may be an important bridge between lymphatic function modulation and inflammation.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058475

DOI: 10.1111/j.1549-8719.2010.00064.x
PubMed: 21166923
PubMed Central: 3058475

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PMC:3058475

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<author><name sortKey="Chakraborty, Sanjukta" sort="Chakraborty, Sanjukta" uniqKey="Chakraborty S" first="Sanjukta" last="Chakraborty">Sanjukta Chakraborty</name>
<affiliation wicri:level="2"><nlm:aff id="A1"> Department of Systems Biology and Translational Medicine, Cardiovascular Research Institute, Division of Lymphatic Biology, Texas A&M Health Science Center College of Medicine, 336 Reynolds Medical Building, College Station, TX</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Texas</region>
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<wicri:cityArea> Department of Systems Biology and Translational Medicine, Cardiovascular Research Institute, Division of Lymphatic Biology, Texas A&M Health Science Center College of Medicine, 336 Reynolds Medical Building, College Station</wicri:cityArea>
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<author><name sortKey="Nepiyushchikh, Zhanna" sort="Nepiyushchikh, Zhanna" uniqKey="Nepiyushchikh Z" first="Zhanna" last="Nepiyushchikh">Zhanna Nepiyushchikh</name>
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<author><name sortKey="Chakraborty, Sanjukta" sort="Chakraborty, Sanjukta" uniqKey="Chakraborty S" first="Sanjukta" last="Chakraborty">Sanjukta Chakraborty</name>
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<author><name sortKey="Nepiyushchikh, Zhanna" sort="Nepiyushchikh, Zhanna" uniqKey="Nepiyushchikh Z" first="Zhanna" last="Nepiyushchikh">Zhanna Nepiyushchikh</name>
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<affiliation wicri:level="2"><nlm:aff id="A1"> Department of Systems Biology and Translational Medicine, Cardiovascular Research Institute, Division of Lymphatic Biology, Texas A&M Health Science Center College of Medicine, 336 Reynolds Medical Building, College Station, TX</nlm:aff>
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<series><title level="j">Microcirculation (New York, N.Y. : 1994)</title>
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<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Objective</title>
<p id="P1">The aim of this study was to elucidate the molecular signaling mechanisms by which substance P (SP) modulates lymphatic muscle contraction and to determine whether SP stimulates both contractile as well as inflammatory pathways in the lymphatics.</p>
</sec>
<sec sec-type="methods" id="S2"><title>Methods</title>
<p id="P2">A rat mesenteric lymphatic muscle cell culture model (RMLMCs) and known specific pharmacological inhibitors were utilized to delineate SP mediated signaling pathways in lymphatics.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">We detected expression of neurokinin receptor 1 (NK1R) and neurokinin receptor 3 (NK3R) in RMLMCs. SP stimulation increased phosphorylation of myosin light chain 20 (MLC<sub>20</sub>
) as well as p38 mitogen associated protein kinase (p38-MAPK) and extracellular signal regulated kinase (ERK1/2) indicating activation of both a contractile and a pro-inflammatory MAPK pathway. Pharmacological inhibition of both NK1R and NK3R significantly affected the downstream SP signaling. We further examined whether there was any crosstalk between the two pathways upon SP stimulation. Inhibition of ERK1/2 decreased levels of p-MLC<sub>20</sub>
 after SP activation, in a PKC dependent manner, indicating a potential crosstalk between these two pathways.</p>
</sec>
<sec id="S4"><title>Conclusions</title>
<p id="P4">These data provide the first evidence that SP mediated crosstalk between pro-inflammatory and contractile signaling mechanisms exists in the lymphatic system and may be an important bridge between lymphatic function modulation and inflammation.</p>
</sec>
</div>
</front>
</TEI>
<pmc article-type="research-article" xml:lang="EN"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
  <pmc-dir>properties manuscript</pmc-dir>
  <front><journal-meta><journal-id journal-id-type="nlm-journal-id">9434935</journal-id>
<journal-id journal-id-type="pubmed-jr-id">8801</journal-id>
<journal-id journal-id-type="nlm-ta">Microcirculation</journal-id>
<journal-title>Microcirculation (New York, N.Y. : 1994)</journal-title>
<issn pub-type="ppub">1073-9688</issn>
<issn pub-type="epub">1549-8719</issn>
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<article-meta><article-id pub-id-type="pmid">21166923</article-id>
<article-id pub-id-type="pmc">3058475</article-id>
<article-id pub-id-type="doi">10.1111/j.1549-8719.2010.00064.x</article-id>
<article-id pub-id-type="manuscript">NIHMS246545</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Substance P activates both contractile and inflammatory pathways in lymphatics through the neurokinin receptors NK1R and NK3R</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Chakraborty</surname>
<given-names>Sanjukta</given-names>
</name>
<xref rid="A1" ref-type="aff">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Nepiyushchikh</surname>
<given-names>Zhanna</given-names>
</name>
<xref rid="A1" ref-type="aff">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Davis</surname>
<given-names>Michael J.</given-names>
</name>
<xref rid="A2" ref-type="aff">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zawieja</surname>
<given-names>David C.</given-names>
</name>
<xref rid="A1" ref-type="aff">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Muthuchamy</surname>
<given-names>Mariappan</given-names>
</name>
<xref rid="A1" ref-type="aff">1</xref>
<xref rid="FN1" ref-type="author-notes">*</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>1</label>
 Department of Systems Biology and Translational Medicine, Cardiovascular Research Institute, Division of Lymphatic Biology, Texas A&M Health Science Center College of Medicine, 336 Reynolds Medical Building, College Station, TX</aff>
<aff id="A2"><label>2</label>
 Department of Medical Pharmacology & Physiology, University of Missouri School of Medicine, Columbia, MO</aff>
<author-notes><corresp id="FN1"><label>*</label>
Correspondence: Mariappan Muthuchamy, Department of Systems Biology and Translational Medicine, Texas A&M Health Science Center College of Medicine, 336 Reynolds Medical Building, College Station, TX 77843, Phone: 979-845-7816, Fax: 979-862-4638, <email>marim@tamu.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>20</day>
<month>10</month>
<year>2010</year>
</pub-date>
<pub-date pub-type="ppub"><month>1</month>
<year>2011</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>1</day>
<month>1</month>
<year>2012</year>
</pub-date>
<volume>18</volume>
<issue>1</issue>
<fpage>24</fpage>
<lpage>35</lpage>
<abstract><sec id="S1"><title>Objective</title>
<p id="P1">The aim of this study was to elucidate the molecular signaling mechanisms by which substance P (SP) modulates lymphatic muscle contraction and to determine whether SP stimulates both contractile as well as inflammatory pathways in the lymphatics.</p>
</sec>
<sec sec-type="methods" id="S2"><title>Methods</title>
<p id="P2">A rat mesenteric lymphatic muscle cell culture model (RMLMCs) and known specific pharmacological inhibitors were utilized to delineate SP mediated signaling pathways in lymphatics.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">We detected expression of neurokinin receptor 1 (NK1R) and neurokinin receptor 3 (NK3R) in RMLMCs. SP stimulation increased phosphorylation of myosin light chain 20 (MLC<sub>20</sub>
) as well as p38 mitogen associated protein kinase (p38-MAPK) and extracellular signal regulated kinase (ERK1/2) indicating activation of both a contractile and a pro-inflammatory MAPK pathway. Pharmacological inhibition of both NK1R and NK3R significantly affected the downstream SP signaling. We further examined whether there was any crosstalk between the two pathways upon SP stimulation. Inhibition of ERK1/2 decreased levels of p-MLC<sub>20</sub>
 after SP activation, in a PKC dependent manner, indicating a potential crosstalk between these two pathways.</p>
</sec>
<sec id="S4"><title>Conclusions</title>
<p id="P4">These data provide the first evidence that SP mediated crosstalk between pro-inflammatory and contractile signaling mechanisms exists in the lymphatic system and may be an important bridge between lymphatic function modulation and inflammation.</p>
</sec>
</abstract>
<kwd-group><kwd>Lymphatic muscle cells</kwd>
<kwd>Substance P</kwd>
<kwd>Neurokinin receptors</kwd>
<kwd>Myosin light chain 20 phosphorylation</kwd>
<kwd>MAP kinase pathways</kwd>
</kwd-group>
<contract-num rid="HL1">R01 HL089784-01A1
				||HL</contract-num>
<contract-num rid="HL1">R01 HL080526-05
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<contract-num rid="HL1">K02 HL086650-03
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<contract-sponsor id="HL1">National Heart, Lung, and Blood Institute  : NHLBI</contract-sponsor>
</article-meta>
</front>
</pmc>
</record>

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Substance P activates both contractile and inflammatory pathways in lymphatics through the neurokinin receptors NK1R and NK3R

Substance P activates both contractile and inflammatory pathways in lymphatics through the neurokinin receptors NK1R and NK3R

Source :

Abstract

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