Thyroid hormone‐induced morphological differentiation and maturation of astrocytes involves activation of protein kinase A and ERK signalling pathway

Ghosh, Mausam; Gharami, Kusumika; Paul, Surojit; Das, Sumantra

doi:10.1111/j.1460-9568.2005.04351.x

Cited by 32 publications

(14 citation statements)

References 63 publications

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“…Cytokine-induced myeloid differentiation is dependent on the activation of the MEK/ERK pathway [33]. Thyroid hormone-induced morphological differentiation and maturation of astrocytes involves an initial decline in the p-ERK level and then sustained activation of p-ERK levels [34]. G proteins and ERK activation play roles in the hemin-induced erythroid differentiation of K562 cells [35].…”

Section: Discussionmentioning

confidence: 99%

Erk is involved in the differentiation induced by diallyl disulfide in the human gastric cancer cell line MGC803

Ling¹,

Zhang²,

Qi³

et al. 2006

Cellular and Molecular Biology Letters

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Diallyl disulfide (DADS) is a major constituent of garlic. Previously, we found that DADS both inhibited proliferation in human gastric cancer cells in vitro and in vivo, and induced G2/M arrest. In this study, we investigated whether this differentiation effect was induced by DADS in human gastric cancer MGC803 cells, and whether it was related to an alteration in ERK activity. The results showed that the growth of MGC803 cells was inhibited by DADS. Cells treated with DADS displayed a lower nucleocytoplasmic ratio and tended to form gland and intercellular conjunction structures. The ConAmediated cell agglutination ratio and cells' ALP specific activity decreased. In MGC803 cells, dye transfer was limited to a few cells neighbouring the dyeinjected cell and to a depth of 1-2 layers beneath the scrape site. However, after treatment with DADS, the LY (Lucifer Yellow) was transferred to several cells immediately neighbouring the microinjected cell and to a depth of 2-4 cell layers from the scrape site. This indicated that DADS induced differentiation in MGC803 cells. Western blot analysis revealed that although DADS did not influence the quantity of ERK1/2 protein expressed, it did decrease its phosphorylation in a concentration-dependent manner, compared with the controls. At 30 mg·L -1 , DADS inhibited the activation of ERK1/2 in 15-30 min. These results suggested that the DADS-induced differentiation of MGC803 cells involved an alteration of the ERK1/2 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Erk is involved in the differentiation induced by diallyl disulfide in the human gastric cancer cell line MGC803

Ling¹,

Zhang²,

Qi³

et al. 2006

Cellular and Molecular Biology Letters

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“…3A). In our earlier studies (Ghosh et al 2005) we had reported that the effect of thyroid hormone on astrocyte differentiation was observed by 24 h after addition of the hormone. Hence, we also looked at the b 2 -AR mRNA levels during 2-24 h, after thyroid hormone administration to the hypothyroid astrocytes.…”

Section: Thyroid Hormone Did Not Change B 2 -Ar Mrna Levels In Astrocmentioning

confidence: 93%

“…Reports from our laboratory showed the effect of thyroid hormone on morphological maturation of astrocytes along with the expression and phosphorylation of vimentin variants (Paul et al 1999) as well as actin biogenesis and polymerization (Paul et al 1996). In a recent study, we have also observed that the effect of thyroid hormone on the maturation of astrocytes is invariably associated with a sustained activation of mitogen activated protein kinase (MAPK) (extracellular signal regulated kinase; ERK) activity (Ghosh et al 2005).…”

Section: Introductionmentioning

confidence: 91%

Increased β2-Adrenergic Receptor Activity by Thyroid Hormone Possibly Leads to Differentiation and Maturation of Astrocytes in Culture

Ghosh

Das

2007

Cell Mol Neurobiol

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(1) Our earlier studies indicate a downsteam regulatory role of the beta-adrenergic receptor (beta-AR) system in thyroid hormone induced differentiation and maturation of astrocytes. In the present study we have investigated the contributions of the subtypes of beta-AR in the above phenomenon. (2) Primary astrocyte cultures were grown under thyroid hormone deficient as well as under euthyroid conditions. [(125)I]Pindolol ([(125)I]PIN) binding studies showed a gradual increase in the specific binding to beta(2)-AR when observed at 5, 10, 15, and 20 days under both cultural conditions. Thyroid hormone caused an increase in binding of [(125)I]PIN to beta(2)-AR compared to thyroid hormone deficient controls at all ages of astrocyte culture. (3) Saturation studies using [(125)I]PIN in astrocyte membranes prepared from 20-day-old cultures showed a significant increase in the affinity of the receptors (K (D)) in the thyroid hormone treated cells without any change in receptor number (B (max)). (4) beta(2)-AR mRNA levels were measured by real-time PCR during ontogenic development as well as during exposure of 10-day-old hypothyroid cultures to normal levels of thyroid hormone for 2, 6, 12, and 24 h. None of the conditions caused any significant change in the beta(2)-adrenergic receptor mRNA levels when compared with corresponding hypothyroid controls. (5) Over expression of beta(2)-AR cDNA in hypothyroid astrocytes caused morphological transformation in spite of the absence of thyroid hormone in the medium. (6) Taken together, results suggest thyroid hormone causes a selective increase in [(125)I]PIN binding to beta(2)-AR due to increase in receptor affinity, which may lead to maturation of astrocytes.

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“…Manipulation of CREB causes drastic changes in L-LTP (Bourtchuladze et al, 1994), and thyroid hormone treatment of neural cells is associated with increased phosphorylation (activation) of CREB at serine-133 position (Ghosh et al, 2005). We hypothesize that reduced CREB levels could explain the impaired L-LTP and long-term memory reported during hypothyroidism (Gerges and Alkadhi, 2004;Gerges et al, 2004b;.…”

Section: Basal Protein Levels Of P-creb and Total Crebmentioning

confidence: 97%

Nicotine prevents disruption of the late phase LTP‐related molecular cascade in adult‐onset hypothyroidism

2007

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We have shown previously that chronic nicotine treatment reverses adult-onset hypothyroidism-induced impairment of late-phase long-term potentiation (L-LTP) in area CA1 of the hippocampus. In the present study, basal and stimulated levels of signaling molecules essential for the expression of L-LTP were determined in area CA1. Immunoblots analysis showed that chronic nicotine treatment of hypothyroid rats prevented the reduction in the basal protein levels of adenylyl cyclase I (ACI), mitogen-activated protein kinases [MAPKp44/42 (ERK1/2)], calcium-calmodulin-dependent protein kinase IV (CaMKIV), and cyclic-AMP response element binding protein [CREB; phosphorylated (P-) and total]. A significant increase in the levels of P-CREB, P-MAPKp44, P-MAPKp42 and brain derived neurotrophic factor (BDNF) was seen 4 h after multiple train high frequency stimulation (MHFS) in nicotine-treated hypothyroid and control animals, but not in hypothyroid animals. The levels of total CREB, total MAPKp44, total MAPKp42, and CaMKIV were elevated in all groups 4 h after MHFS. These findings suggest that prevention of the reduced basal level of CaMKIV, MAPKp44/42, and CREB by nicotine along with the regained ability of MHFS to induce MAPKp44/42 and CREB phosphorylation in nicotine treated hypothyroid animals may be responsible for the reversal of L-LTP impairment by chronic nicotine treatment in this disease model.

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Thyroid hormone‐induced morphological differentiation and maturation of astrocytes involves activation of protein kinase A and ERK signalling pathway

Cited by 32 publications

References 63 publications

Erk is involved in the differentiation induced by diallyl disulfide in the human gastric cancer cell line MGC803

Erk is involved in the differentiation induced by diallyl disulfide in the human gastric cancer cell line MGC803

Increased β2-Adrenergic Receptor Activity by Thyroid Hormone Possibly Leads to Differentiation and Maturation of Astrocytes in Culture

Nicotine prevents disruption of the late phase LTP‐related molecular cascade in adult‐onset hypothyroidism

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