Phospholipase C-β3 mediates the thrombin-induced Ca2+ response in glial cells

Jong-Ik Hwang, Kum Joo Shin, Yong Seok Oh, Jung Woong Choi, Zee Won Lee, Daesoo Kim, Kwon Soo Ha, Hee Sup Shin, Sung Ho Ryu, Pann Ghill Suh

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Phospholipase C-β (PLC-β) hydrolyses phosphatidylinositol 4,5-bisphosphate and generates inositol 1,4,5-trisphosphate in response to activation of various G protein-coupled receptors (GPCRs). Using glial cells from knock-out mice lacking either PLC-β1 [PLC-β1 (-/-)] or PLC-β3 [PLC-β3 (-/-)], we examined which isotype of PLC- participated in the cellular signaling events triggered by thrombin. Generation of inositol phosphates (IPs) was enhanced by thrombin in PLC-β1 (-/-) cells, but was negligible in PLC-β3 (-/-) cells. Expression of PLC-β in PLC-β(-/-) cells resulted in an increase in pertussis toxin (PTx)-sensitive IPs in response to thrombin as well as to PARI-specific peptide, while expression of PLC-β1 in PLC-β1 (-/-) cells did not have any effect on IP generation. The thrombin-induced [Ca2+]i increase was delayed and attenuated in PLC-β3 (-/-) cells, but normal in PLC-β1 (-/-) cells. Pertussis toxin evoked a delayed [Ca2+], increase in PLC-β3 (-/-) cells as well as in PLC-β1 (-/-) cells. These results suggest that activation of PLC-β3 by pertussis toxin-sensitive G proteins is responsible for the transient [Ca2+], increase in response to thrombin, whereas the delayed [Ca2+], increase may be due to activation of some other PLC, such as PLC-β4, acting via PTx-insensitive G proteins.

Original languageEnglish
Pages (from-to)375-381
Number of pages7
JournalMolecules and Cells
Volume19
Issue number3
DOIs
Publication statusPublished - 2005 Dec 1
Externally publishedYes

Fingerprint

Type C Phospholipases
Thrombin
Neuroglia
Pertussis Toxin
Inositol Phosphates
GTP-Binding Proteins
Inositol 1,4,5-Trisphosphate
G-Protein-Coupled Receptors
Phosphatidylinositols

Keywords

  • Calcium
  • Glial Cells Inositol Phosphates
  • GPCR
  • PLC-β3

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cell Biology

Cite this

Phospholipase C-β3 mediates the thrombin-induced Ca2+ response in glial cells. / Hwang, Jong-Ik; Shin, Kum Joo; Oh, Yong Seok; Choi, Jung Woong; Lee, Zee Won; Kim, Daesoo; Ha, Kwon Soo; Shin, Hee Sup; Ryu, Sung Ho; Suh, Pann Ghill.

In: Molecules and Cells, Vol. 19, No. 3, 01.12.2005, p. 375-381.

Research output: Contribution to journalArticle

Hwang, J-I, Shin, KJ, Oh, YS, Choi, JW, Lee, ZW, Kim, D, Ha, KS, Shin, HS, Ryu, SH & Suh, PG 2005, 'Phospholipase C-β3 mediates the thrombin-induced Ca2+ response in glial cells', Molecules and Cells, vol. 19, no. 3, pp. 375-381. https://doi.org/10.1016/j.atherosclerosis.2004.12.046
Hwang, Jong-Ik ; Shin, Kum Joo ; Oh, Yong Seok ; Choi, Jung Woong ; Lee, Zee Won ; Kim, Daesoo ; Ha, Kwon Soo ; Shin, Hee Sup ; Ryu, Sung Ho ; Suh, Pann Ghill. / Phospholipase C-β3 mediates the thrombin-induced Ca2+ response in glial cells. In: Molecules and Cells. 2005 ; Vol. 19, No. 3. pp. 375-381.
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AU - Hwang, Jong-Ik

AU - Shin, Kum Joo

AU - Oh, Yong Seok

AU - Choi, Jung Woong

AU - Lee, Zee Won

AU - Kim, Daesoo

AU - Ha, Kwon Soo

AU - Shin, Hee Sup

AU - Ryu, Sung Ho

AU - Suh, Pann Ghill

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N2 - Phospholipase C-β (PLC-β) hydrolyses phosphatidylinositol 4,5-bisphosphate and generates inositol 1,4,5-trisphosphate in response to activation of various G protein-coupled receptors (GPCRs). Using glial cells from knock-out mice lacking either PLC-β1 [PLC-β1 (-/-)] or PLC-β3 [PLC-β3 (-/-)], we examined which isotype of PLC- participated in the cellular signaling events triggered by thrombin. Generation of inositol phosphates (IPs) was enhanced by thrombin in PLC-β1 (-/-) cells, but was negligible in PLC-β3 (-/-) cells. Expression of PLC-β in PLC-β(-/-) cells resulted in an increase in pertussis toxin (PTx)-sensitive IPs in response to thrombin as well as to PARI-specific peptide, while expression of PLC-β1 in PLC-β1 (-/-) cells did not have any effect on IP generation. The thrombin-induced [Ca2+]i increase was delayed and attenuated in PLC-β3 (-/-) cells, but normal in PLC-β1 (-/-) cells. Pertussis toxin evoked a delayed [Ca2+], increase in PLC-β3 (-/-) cells as well as in PLC-β1 (-/-) cells. These results suggest that activation of PLC-β3 by pertussis toxin-sensitive G proteins is responsible for the transient [Ca2+], increase in response to thrombin, whereas the delayed [Ca2+], increase may be due to activation of some other PLC, such as PLC-β4, acting via PTx-insensitive G proteins.

AB - Phospholipase C-β (PLC-β) hydrolyses phosphatidylinositol 4,5-bisphosphate and generates inositol 1,4,5-trisphosphate in response to activation of various G protein-coupled receptors (GPCRs). Using glial cells from knock-out mice lacking either PLC-β1 [PLC-β1 (-/-)] or PLC-β3 [PLC-β3 (-/-)], we examined which isotype of PLC- participated in the cellular signaling events triggered by thrombin. Generation of inositol phosphates (IPs) was enhanced by thrombin in PLC-β1 (-/-) cells, but was negligible in PLC-β3 (-/-) cells. Expression of PLC-β in PLC-β(-/-) cells resulted in an increase in pertussis toxin (PTx)-sensitive IPs in response to thrombin as well as to PARI-specific peptide, while expression of PLC-β1 in PLC-β1 (-/-) cells did not have any effect on IP generation. The thrombin-induced [Ca2+]i increase was delayed and attenuated in PLC-β3 (-/-) cells, but normal in PLC-β1 (-/-) cells. Pertussis toxin evoked a delayed [Ca2+], increase in PLC-β3 (-/-) cells as well as in PLC-β1 (-/-) cells. These results suggest that activation of PLC-β3 by pertussis toxin-sensitive G proteins is responsible for the transient [Ca2+], increase in response to thrombin, whereas the delayed [Ca2+], increase may be due to activation of some other PLC, such as PLC-β4, acting via PTx-insensitive G proteins.

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KW - Glial Cells Inositol Phosphates

KW - GPCR

KW - PLC-β3

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