schliessen

Filtern

 

Bibliotheken

Ca 2+ -CaMKKβ pathway is required for adiponectin-induced secretion in rat submandibular gland

Adiponectin functions as a promoter of saliva secretion in rat submandibular gland via activation of adenosine monophosphate-activated protein kinase (AMPK) and increased paracellular permeability. Ca 2+ mobilization is the primary signal for fluid secretion in salivary acinar cells. However, whethe... Full description

Journal Title: Journal of Molecular Histology 2018, Vol.49(1), pp.99-110
Main Author: Ding, Chong
Other Authors: Du, Zhi-Hao , Li, Sheng-Lin , Wu, Li-Ling , Yu, Guang-Yan
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 1567-2379 ; E-ISSN: 1567-2387 ; DOI: 10.1007/s10735-017-9750-3
Link: http://dx.doi.org/10.1007/s10735-017-9750-3
Zum Text:
SendSend as email Add to Book BagAdd to Book Bag
Staff View
recordid: springer_jour10.1007/s10735-017-9750-3
title: Ca 2+ -CaMKKβ pathway is required for adiponectin-induced secretion in rat submandibular gland
format: Article
creator:
  • Ding, Chong
  • Du, Zhi-Hao
  • Li, Sheng-Lin
  • Wu, Li-Ling
  • Yu, Guang-Yan
subjects:
  • Adiponectin
  • Calcium
  • Calcium/calmodulin-dependent protein kinase
  • Adenosine monophosphate-activated protein kinase
  • Submandibular gland
  • Secretion
ispartof: Journal of Molecular Histology, 2018, Vol.49(1), pp.99-110
description: Adiponectin functions as a promoter of saliva secretion in rat submandibular gland via activation of adenosine monophosphate-activated protein kinase (AMPK) and increased paracellular permeability. Ca 2+ mobilization is the primary signal for fluid secretion in salivary acinar cells. However, whether intracellular Ca 2+ mobilization is involved in adiponectin-induced salivary secretion is unknown. Here, we found that full-length adiponectin (fAd) increased intracellular Ca 2+ and saliva secretion in submandibular glands. Pre-perfusion with ethylene glycol-bis (2-aminoethylether)- N,N,N′,N′ -tetraacetic acid (EGTA) combined with thapsigargin (TG), an endoplasmic reticulum Ca 2+ -ATPase inhibitor, abolished fAd-induced salivary secretion, AMPK phosphorylation, and enlarged tight junction (TJ) width. Furthermore, in cultured SMG-C6 cells, co-pretreatment with EGTA and TG suppressed fAd-decreased transepithelial electrical resistance and increased 4-kDa FITC-dextran flux responses. Moreover, fAd increased phosphorylation of calcium/calmodulin-dependent protein kinase (CaMKKβ), a major kinase that is activated by elevated levels of intracellular Ca 2+ , but not liver kinase B1 phosphorylation. Pre-perfusion of the isolated gland with STO-609, an inhibitor of CaMKKβ, abolished fAd-induced salivary secretion, AMPK activation, and enlarged TJ width. CaMKKβ shRNA suppressed, whereas CaMKKβ re-expression rescued fAd-increased paracellular permeability. Taken together, these results indicate that adiponectin induced Ca 2+ modulation in rat submandibular gland acinar cells. Ca 2+ -CaMKKβ pathway is required for adiponectin-induced secretion through mediating AMPK activation and increase in paracellular permeability in rat submandibular glands.
language: eng
source:
identifier: ISSN: 1567-2379 ; E-ISSN: 1567-2387 ; DOI: 10.1007/s10735-017-9750-3
fulltext: fulltext
issn:
  • 1567-2387
  • 15672387
  • 1567-2379
  • 15672379
url: Link


@attributes
ID135630872
RANK0.07
NO1
SEARCH_ENGINEprimo_central_multiple_fe
SEARCH_ENGINE_TYPEPrimo Central Search Engine
LOCALfalse
PrimoNMBib
record
control
sourcerecordid10.1007/s10735-017-9750-3
sourceidspringer_jour
recordidTN_springer_jour10.1007/s10735-017-9750-3
sourcesystemPC
pqid1977092739
galeid521174454
display
typearticle
titleCa 2+ -CaMKKβ pathway is required for adiponectin-induced secretion in rat submandibular gland
creatorDing, Chong ; Du, Zhi-Hao ; Li, Sheng-Lin ; Wu, Li-Ling ; Yu, Guang-Yan
ispartofJournal of Molecular Histology, 2018, Vol.49(1), pp.99-110
identifier
subjectAdiponectin ; Calcium ; Calcium/calmodulin-dependent protein kinase ; Adenosine monophosphate-activated protein kinase ; Submandibular gland ; Secretion
descriptionAdiponectin functions as a promoter of saliva secretion in rat submandibular gland via activation of adenosine monophosphate-activated protein kinase (AMPK) and increased paracellular permeability. Ca 2+ mobilization is the primary signal for fluid secretion in salivary acinar cells. However, whether intracellular Ca 2+ mobilization is involved in adiponectin-induced salivary secretion is unknown. Here, we found that full-length adiponectin (fAd) increased intracellular Ca 2+ and saliva secretion in submandibular glands. Pre-perfusion with ethylene glycol-bis (2-aminoethylether)- N,N,N′,N′ -tetraacetic acid (EGTA) combined with thapsigargin (TG), an endoplasmic reticulum Ca 2+ -ATPase inhibitor, abolished fAd-induced salivary secretion, AMPK phosphorylation, and enlarged tight junction (TJ) width. Furthermore, in cultured SMG-C6 cells, co-pretreatment with EGTA and TG suppressed fAd-decreased transepithelial electrical resistance and increased 4-kDa FITC-dextran flux responses. Moreover, fAd increased phosphorylation of calcium/calmodulin-dependent protein kinase (CaMKKβ), a major kinase that is activated by elevated levels of intracellular Ca 2+ , but not liver kinase B1 phosphorylation. Pre-perfusion of the isolated gland with STO-609, an inhibitor of CaMKKβ, abolished fAd-induced salivary secretion, AMPK activation, and enlarged TJ width. CaMKKβ shRNA suppressed, whereas CaMKKβ re-expression rescued fAd-increased paracellular permeability. Taken together, these results indicate that adiponectin induced Ca 2+ modulation in rat submandibular gland acinar cells. Ca 2+ -CaMKKβ pathway is required for adiponectin-induced secretion through mediating AMPK activation and increase in paracellular permeability in rat submandibular glands.
languageeng
source
version6
lds50peer_reviewed
links
openurl$$Topenurl_article
openurlfulltext$$Topenurlfull_article
backlink$$Uhttp://dx.doi.org/10.1007/s10735-017-9750-3$$EView_full_text_in_Springer_(Subscribers_only)
search
creatorcontrib
0Ding, Chong
1Du, Zhi-Hao
2Li, Sheng-Lin
3Wu, Li-Ling
4Yu, Guang-Yan
titleCa 2+ -CaMKKβ pathway is required for adiponectin-induced secretion in rat submandibular gland
descriptionAdiponectin functions as a promoter of saliva secretion in rat submandibular gland via activation of adenosine monophosphate-activated protein kinase (AMPK) and increased paracellular permeability. Ca 2+ mobilization is the primary signal for fluid secretion in salivary acinar cells. However, whether intracellular Ca 2+ mobilization is involved in adiponectin-induced salivary secretion is unknown. Here, we found that full-length adiponectin (fAd) increased intracellular Ca 2+ and saliva secretion in submandibular glands. Pre-perfusion with ethylene glycol-bis (2-aminoethylether)- N,N,N′,N′ -tetraacetic acid (EGTA) combined with thapsigargin (TG), an endoplasmic reticulum Ca 2+ -ATPase inhibitor, abolished fAd-induced salivary secretion, AMPK phosphorylation, and enlarged tight junction (TJ) width. Furthermore, in cultured SMG-C6 cells, co-pretreatment with EGTA and TG suppressed fAd-decreased transepithelial electrical resistance and increased 4-kDa FITC-dextran flux responses. Moreover, fAd increased phosphorylation of calcium/calmodulin-dependent protein kinase (CaMKKβ), a major kinase that is activated by elevated levels of intracellular Ca 2+ , but not liver kinase B1 phosphorylation. Pre-perfusion of the isolated gland with STO-609, an inhibitor of CaMKKβ, abolished fAd-induced salivary secretion, AMPK activation, and enlarged TJ width. CaMKKβ shRNA suppressed, whereas CaMKKβ re-expression rescued fAd-increased paracellular permeability. Taken together, these results indicate that adiponectin induced Ca 2+ modulation in rat submandibular gland acinar cells. Ca 2+ -CaMKKβ pathway is required for adiponectin-induced secretion through mediating AMPK activation and increase in paracellular permeability in rat submandibular glands.
subject
0Adiponectin
1Calcium
2Calcium/calmodulin-dependent protein kinase
3Adenosine monophosphate-activated protein kinase
4Submandibular gland
5Secretion
general
010.1007/s10735-017-9750-3
1English
2Springer Science & Business Media B.V.
3SpringerLink
sourceidspringer_jour
recordidspringer_jour10.1007/s10735-017-9750-3
issn
01567-2387
115672387
21567-2379
315672379
rsrctypearticle
creationdate2018
addtitle
0Journal of Molecular Histology
1J Mol Hist
searchscopespringer_journals_complete
scopespringer_journals_complete
lsr30VSR-Enriched:[pages, orcidid, pqid, galeid]
sort
titleCa 2+ -CaMKKβ pathway is required for adiponectin-induced secretion in rat submandibular gland
authorDing, Chong ; Du, Zhi-Hao ; Li, Sheng-Lin ; Wu, Li-Ling ; Yu, Guang-Yan
creationdate20180200
facets
frbrgroupid4246803721275318028
frbrtype5
newrecords20180110
languageeng
creationdate2018
topic
0Adiponectin
1Calcium
2Calcium/Calmodulin-Dependent Protein Kinase
3Adenosine Monophosphate-Activated Protein Kinase
4Submandibular Gland
5Secretion
collectionSpringerLink
prefilterarticles
rsrctypearticles
creatorcontrib
0Ding, Chong
1Du, Zhi-Hao
2Li, Sheng-Lin
3Wu, Li-Ling
4Yu, Guang-Yan
jtitleJournal Of Molecular Histology
toplevelpeer_reviewed
delivery
delcategoryRemote Search Resource
fulltextfulltext
addata
aulast
0Ding
1Du
2Li
3Wu
4Yu
aufirst
0Chong
1Zhi-Hao
2Sheng-Lin
3Li-Ling
4Guang-Yan
au
0Ding, Chong
1Du, Zhi-Hao
2Li, Sheng-Lin
3Wu, Li-Ling
4Yu, Guang-Yan
atitleCa 2+ -CaMKKβ pathway is required for adiponectin-induced secretion in rat submandibular gland
jtitleJournal of Molecular Histology
stitleJ Mol Hist
risdate201802
volume49
issue1
spage99
epage110
issn1567-2379
eissn1567-2387
genrearticle
ristypeJOUR
abstractAdiponectin functions as a promoter of saliva secretion in rat submandibular gland via activation of adenosine monophosphate-activated protein kinase (AMPK) and increased paracellular permeability. Ca 2+ mobilization is the primary signal for fluid secretion in salivary acinar cells. However, whether intracellular Ca 2+ mobilization is involved in adiponectin-induced salivary secretion is unknown. Here, we found that full-length adiponectin (fAd) increased intracellular Ca 2+ and saliva secretion in submandibular glands. Pre-perfusion with ethylene glycol-bis (2-aminoethylether)- N,N,N′,N′ -tetraacetic acid (EGTA) combined with thapsigargin (TG), an endoplasmic reticulum Ca 2+ -ATPase inhibitor, abolished fAd-induced salivary secretion, AMPK phosphorylation, and enlarged tight junction (TJ) width. Furthermore, in cultured SMG-C6 cells, co-pretreatment with EGTA and TG suppressed fAd-decreased transepithelial electrical resistance and increased 4-kDa FITC-dextran flux responses. Moreover, fAd increased phosphorylation of calcium/calmodulin-dependent protein kinase (CaMKKβ), a major kinase that is activated by elevated levels of intracellular Ca 2+ , but not liver kinase B1 phosphorylation. Pre-perfusion of the isolated gland with STO-609, an inhibitor of CaMKKβ, abolished fAd-induced salivary secretion, AMPK activation, and enlarged TJ width. CaMKKβ shRNA suppressed, whereas CaMKKβ re-expression rescued fAd-increased paracellular permeability. Taken together, these results indicate that adiponectin induced Ca 2+ modulation in rat submandibular gland acinar cells. Ca 2+ -CaMKKβ pathway is required for adiponectin-induced secretion through mediating AMPK activation and increase in paracellular permeability in rat submandibular glands.
copDordrecht
pubSpringer Netherlands
doi10.1007/s10735-017-9750-3
pages99-110
orcididhttp://orcid.org/0000-0002-1834-4421
date2018-02