Vitamin D regulates contractile profile in human uterine myometrial cells via NF-κB pathway

Chandrasekhar Thota, Archana Laknaur, Takeisha Farmer, Gwinnett Ladson, Ayman Al-Hendy, Nahed Ismail

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Objective Infection triggers inflammation that, in turn, enhances the expression of contractile-associated factors in myometrium and increases the risk of preterm delivery. In this study, we assessed vitamin D regulation of inflammatory markers, contractile-associated factors, steroid hormone receptors, and NFκB pathway proteins in human uterine myometrial smooth muscle (UtSM) cells that were cultured in an inflammatory environment. Study Design Inflammatory environment was simulated for UtSM cells by coculturing them with monocyte lineage (THP1) cells. We measured the expression of inflammatory markers, contractile-associated factors, steroid hormone receptors, and NFκB pathway proteins in UtSM cells that were cultured with THP1 cells in the presence and absence of vitamin D by real time polymerase chain reaction and Western blot analysis. Results Monocytes secreted monocyte inflammatory protein-1α and -1β, interleukin (IL)-1β and 6, and tumor necrosis factor-α into the conditioned medium. In the UtSM cells that had been cocultured with THP1 cells, there was a significant (P <.05) increase in the expression of inflammatory markers IL-1β, -6, and -13 and tumor necrosis factor-α; the contractile-associated factors connexin-43, Cox-2, and prostaglandin F 2 α receptor; the estrogen receptor α, and progesterone receptors A and B. Vitamin D treatment of cocultures decreased (P <.05) the expression of inflammatory markers and contractile-associated factors in UtSM cells. Similarly, vitamin D decreased estrogen receptor α and progesterone receptors A-to-B ratio in UtSM cells that were cocultured with THP1 cells. In addition, vitamin D treatment significantly (P <.05) decreased monocyte-induced p-IκBα in cytosol and NFκB-p65 in the nucleus and increased IκBα in cytosol in UtSM cells. Conclusion Our results suggest that vitamin D treatment decreases inflammation-induced cytokines and contractile-associated factors in the uterine myometrial smooth muscle cells through the NFκB pathway.

Original languageEnglish (US)
Pages (from-to)347.e1-347.e10
JournalAmerican Journal of Obstetrics and Gynecology
Volume210
Issue number4
DOIs
StatePublished - Jan 1 2014

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Vitamin D
Smooth Muscle Myocytes
Monocytes
Steroid Receptors
Interleukin-1
Estrogen Receptors
Cytosol
Interleukin-6
Tumor Necrosis Factor-alpha
Environment Design
Hormones
Inflammation
Vitamin B Complex
Connexin 43
Proteins
Myometrium
Prostaglandins F
Conditioned Culture Medium
Coculture Techniques
Real-Time Polymerase Chain Reaction

Keywords

  • NFκB
  • contractile-associated factor
  • inflammatory marker
  • monocyte
  • myometrial cell

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

Vitamin D regulates contractile profile in human uterine myometrial cells via NF-κB pathway. / Thota, Chandrasekhar; Laknaur, Archana; Farmer, Takeisha; Ladson, Gwinnett; Al-Hendy, Ayman; Ismail, Nahed.

In: American Journal of Obstetrics and Gynecology, Vol. 210, No. 4, 01.01.2014, p. 347.e1-347.e10.

Research output: Contribution to journalArticle

Thota, Chandrasekhar ; Laknaur, Archana ; Farmer, Takeisha ; Ladson, Gwinnett ; Al-Hendy, Ayman ; Ismail, Nahed. / Vitamin D regulates contractile profile in human uterine myometrial cells via NF-κB pathway. In: American Journal of Obstetrics and Gynecology. 2014 ; Vol. 210, No. 4. pp. 347.e1-347.e10.
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AU - Al-Hendy, Ayman

AU - Ismail, Nahed

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N2 - Objective Infection triggers inflammation that, in turn, enhances the expression of contractile-associated factors in myometrium and increases the risk of preterm delivery. In this study, we assessed vitamin D regulation of inflammatory markers, contractile-associated factors, steroid hormone receptors, and NFκB pathway proteins in human uterine myometrial smooth muscle (UtSM) cells that were cultured in an inflammatory environment. Study Design Inflammatory environment was simulated for UtSM cells by coculturing them with monocyte lineage (THP1) cells. We measured the expression of inflammatory markers, contractile-associated factors, steroid hormone receptors, and NFκB pathway proteins in UtSM cells that were cultured with THP1 cells in the presence and absence of vitamin D by real time polymerase chain reaction and Western blot analysis. Results Monocytes secreted monocyte inflammatory protein-1α and -1β, interleukin (IL)-1β and 6, and tumor necrosis factor-α into the conditioned medium. In the UtSM cells that had been cocultured with THP1 cells, there was a significant (P <.05) increase in the expression of inflammatory markers IL-1β, -6, and -13 and tumor necrosis factor-α; the contractile-associated factors connexin-43, Cox-2, and prostaglandin F 2 α receptor; the estrogen receptor α, and progesterone receptors A and B. Vitamin D treatment of cocultures decreased (P <.05) the expression of inflammatory markers and contractile-associated factors in UtSM cells. Similarly, vitamin D decreased estrogen receptor α and progesterone receptors A-to-B ratio in UtSM cells that were cocultured with THP1 cells. In addition, vitamin D treatment significantly (P <.05) decreased monocyte-induced p-IκBα in cytosol and NFκB-p65 in the nucleus and increased IκBα in cytosol in UtSM cells. Conclusion Our results suggest that vitamin D treatment decreases inflammation-induced cytokines and contractile-associated factors in the uterine myometrial smooth muscle cells through the NFκB pathway.

AB - Objective Infection triggers inflammation that, in turn, enhances the expression of contractile-associated factors in myometrium and increases the risk of preterm delivery. In this study, we assessed vitamin D regulation of inflammatory markers, contractile-associated factors, steroid hormone receptors, and NFκB pathway proteins in human uterine myometrial smooth muscle (UtSM) cells that were cultured in an inflammatory environment. Study Design Inflammatory environment was simulated for UtSM cells by coculturing them with monocyte lineage (THP1) cells. We measured the expression of inflammatory markers, contractile-associated factors, steroid hormone receptors, and NFκB pathway proteins in UtSM cells that were cultured with THP1 cells in the presence and absence of vitamin D by real time polymerase chain reaction and Western blot analysis. Results Monocytes secreted monocyte inflammatory protein-1α and -1β, interleukin (IL)-1β and 6, and tumor necrosis factor-α into the conditioned medium. In the UtSM cells that had been cocultured with THP1 cells, there was a significant (P <.05) increase in the expression of inflammatory markers IL-1β, -6, and -13 and tumor necrosis factor-α; the contractile-associated factors connexin-43, Cox-2, and prostaglandin F 2 α receptor; the estrogen receptor α, and progesterone receptors A and B. Vitamin D treatment of cocultures decreased (P <.05) the expression of inflammatory markers and contractile-associated factors in UtSM cells. Similarly, vitamin D decreased estrogen receptor α and progesterone receptors A-to-B ratio in UtSM cells that were cocultured with THP1 cells. In addition, vitamin D treatment significantly (P <.05) decreased monocyte-induced p-IκBα in cytosol and NFκB-p65 in the nucleus and increased IκBα in cytosol in UtSM cells. Conclusion Our results suggest that vitamin D treatment decreases inflammation-induced cytokines and contractile-associated factors in the uterine myometrial smooth muscle cells through the NFκB pathway.

KW - NFκB

KW - contractile-associated factor

KW - inflammatory marker

KW - monocyte

KW - myometrial cell

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