Effect of growth factors and steroid hormones on heme oxygenase and cyclin D1 expression in primary astroglial cell cultures

Abstract

Astrocyte activity may be modulated by steroid hormones and GFs. This study investigates the interaction between glucocorticoids or estrogens and GFs on the expression of heme oxygenase-1 (HO-1) and cyclin D1 in astrocyte cultures at 14 days treated for 48 or 60 hr with dexamethasone (DEX) or 48 hr with 17β-estradiol (E2) alone or with GFs added only in the last 12 or 24 hr. Twelve- or twenty-four-hour epidermal growth factor (EGF) treatment significantly enhanced HO-1 expression in astrocyte cultures pretreated for 48 hr with DEX. A highly significant increase in HO-1 expression was obtained after the last-12-hr EGF treatment in 48-hr E2-pretreated astrocyte cultures; this enhancement was particularly significant in 48-hr E2-pretreated cultures as well as in the last-12-hr insulin-treated ones pretreated for 48 hr with E2. Sixty-hour DEX-alone pretreatment as well as the last-12-hr EGF treatment in 60-hr DEX-pretreated astrocyte cultures showed a significant increase of cyclin D1 expression. A significant decrease of cyclin D1 expression in the last-12-hr insulin-like growth factor-I (IGF-1)-treated cultures pretreated for 60 hr with DEX was observed. A highly significant enhancement in cyclin D1 expression in 14 days in vitro astrocyte cultures pretreated with E2 alone for 48 hr and treated in the last 12 hr with IGF-1 in 48-hr E2-pretreated cultures was found. Finally, the data highlight an interactive dialogue between the growth factors and glucocorticoids or estrogens during the maturation of astroglial cells in culture that may control the HO-1 and cyclin D1 expression as well as proliferating astroglial cells during the cell cycle.

Modulation of extracellular signal‐related kinase, cyclin D1, glial fibrillary acidic protein, and vimentin expression in estradiol‐pretreated astrocyte cultures treated with competence and progression growth factors

“…β‐Actin monoclonal antibody (clone [AC‐15]: antibody ID: AB_367161; antibody name: β‐actin antibody [AC‐15]; antibody target: β‐actin antibody [AC‐15]; vendor: GeneTex [Irvine, CA; catalog No: GTX26276]; clonality: monoclonal antibody; clone ID: clone AC‐15; host organism: mouse; Proper Citation: GeneTex [catalog No. GTX26276; RRID: AB_367161]) recognized a single band of 42 kDa molecular weight on Western blots of rat brain (manufacturer's data sheet) and stained a pattern of cellular morphology and distribution identical to that in our previous studies (Bramanti et al, ). Staining was eliminated by preincubation of the diluted antiserum (1:2,000) with 30 µg/ml of the recombinant protein.…”

“…Some findings (Dhandapani and Brann, 2003) support a role for astrocytes in neuroprotection and raise the intriguing possibility that astrocytes might help to mediate the neuroprotective effect of 17b-estradiol (17b-E 2 ) in an in vitro model. GFs, such as basic fibroblast growth factor (bFGF), EGF, IGF-I, and INS, act as mitogenic peptides and participate in neuron-glia cross-talk, stimulating cultured nerve cell proliferation and differentiation (Bramanti et al, 2015). In particular, GFs play a pivotal role in the dynamic flow of signaling molecules between neurons and astroglia (Avola et al, 2000;Bramanti et al, 2015).…”

“…GFs, such as basic fibroblast growth factor (bFGF), EGF, IGF‐I, and INS, act as mitogenic peptides and participate in neuron–glia cross‐talk, stimulating cultured nerve cell proliferation and differentiation (Bramanti et al, ). In particular, GFs play a pivotal role in the dynamic flow of signaling molecules between neurons and astroglia (Avola et al, ; Bramanti et al, ).…”

Corticosterone Inhibits the Proliferation of C6 Glioma Cells <i>via</i> the Translocation of Unphosphorylated Glucocorticoid Receptor

“…As a candidate which is regulated its expression by CORT, cyclin-related proteins, such as cyclin D1, D3, cyclin-dependent kinase 4 or 6, might play a role here, since they are related to cell proliferation and their function is modulated by glucocorticoid. [33][34][35] In conclusion, we demonstrated that CORT inhibited the proliferation of C6 glioma cells via GR, but not MR, by using their respective antagonists, mifepristone and spironolactone. In addition, this inhibitory effect of cell proliferation was unrelated to apoptosis or mitochondrial dysfunction.…”

Monocarboxylate transporter-dependent mechanism confers resistance to oxygen- and glucose-deprivation injury in astrocyte-neuron co-cultures

“…They are the most abundant glial cells in the brain that are closely associated with neuronal synapses [1]. Glial cells are also involved in providing neurotrophic signals to neurons required for their survival, proliferation, and differentiation [2]. In addition, reciprocal interactions between glia and neurons are essential for many critical functions in brain health and disease.…”