Low-level laser irradiation modulates brain-derived neurotrophic factor mRNA transcription through calcium-dependent activation of the ERK/CREB pathway. Issue 1 (January 2017)

• Record Type: Journal Article
• Authors: Yan, Xiaodong; Liu, Juanfang; Zhang, Zhengping; Li, Wenhao; Sun, Siguo; Zhao, Jian; Dong, Xin; Qian, Jixian; Sun, Honghui
• Is Part Of: Lasers in medical science. Volume 32:Issue 1(2017)
• Page Start: 169
• Page End: 180
• Publication Date: 2017-01
• Subjects: Low-level laser -- Brain-derived neurotrophic factor -- Calcium -- Extracellular signal-regulated kinase -- cAMP-response element binding protein; Lasers in medicine -- Periodicals; 610.28
• DOI: 10.1007/s10103-016-2099-0
• Languages: English
• ISSNs: 0268-8921

Abstract

Abstract Low-level laser (LLL) irradiation has been reported to promote neuronal differentiation, but the mechanism remains unclear. Brain-derived neurotrophic factor (BDNF) has been confirmed to be one of the most important neurotrophic factors because it is critical for the differentiation and survival of neurons during development. Thus, this study aimed to investigate the effects of LLL irradiation onBdnf messenger RNA (mRNA) transcription and the molecular pathway involved in LLL-inducedBdnf mRNA transcription in cultured dorsal root ganglion neurons (DRGNs) using Ca2+ imaging, pharmacological detections, RNA interference, immunocytochemistry assay, Western blot, and qPCR analysis. We show here that LLL induced increases in the [Ca2+ ]i level, Bdnf mRNA transcription, cAMP-response element-binding protein (CREB) phosphorylation, and extracellular signal-regulated kinase (ERK) phosphorylation, mediated by Ca2+ release via inositol triphosphate receptor (IP3R)-sensitive calcium (Ca2+ ) stores. Blockade of Ca2+ increase suppressedBdnf mRNA transcription, CREB phosphorylation, and ERK phosphorylation. Downregulation of phosphorylated (p)-CREB reducedBdnf mRNA transcription triggered by LLL. Furthermore, blockade of ERK using PD98059 inhibitor reduced p-CREB andBdnf mRNA transcription induced by LLL. Taken together, these findings establish the Ca2+ -ERK-CREB cascade as a potential signaling pathway involved in LLL-inducedBdnf mRNA transcription. To our knowledge, this is the first report of the mechanisms of Ca2+ -dependentBdnf mRNA transcription triggered by LLL. These findings may help further explore the complex molecular signaling networks in LLL-triggered nerve regeneration in vivo and may also provide experimental evidence for the development of LLL for clinical applications.