Downregulation of TRPM7, TRPM8, and TRPV1 channels modulate apoptotic parameters and neurodegenerative markers: Focus on neuronal differentiation and Parkinson's disease model

Öz, Ahmi; Çelik, Ömer

doi:10.1002/cbin.12048

Cited by 6 publications

(4 citation statements)

References 57 publications

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“…MOG (myelin oligodendrocyte glycoprotein) [431], ERBB3 [432], NHLH2 [433], GADD45B [434], PADI2 [435], ADORA1 [436], NINJ2 [437], WNT7A [438], DAO (D-amino acid oxidase) [439], PRODH (proline dehydrogenase 1) [440] and HCRTR1 [441] could regulate the development of psychiatric disorders. CCR2 [442], FASLG (Fas ligand) [443], GPNMB (glycoprotein nmb) [444], NPY2R [445], TRPM8 [446], TTR (transthyretin) [447], ADM (adrenomedullin) [448], CHI3L1 [375], CDH1 [377], HIP1R [449], SEMA4D [450], HAPLN2 [451], MYRF (myelin regulatory factor) [452], BIN1 [453], BMP2 [454], APLP1 [391], SEPTIN4 [455], DAO (D-amino acid oxidase) [456], TKTL1 [347], ADAP1 [457], HPDL (4-hydroxyphenylpyruvate dioxygenase like) [458], NME3 [459], SPON1 [460] and LGALS3BP [225] were revealed to be altered expressed in neurodegenerative diseases. CCR2 [461], FASLG (Fas ligand) [462], CD28 [463], LYZ (lysozyme) [464], CCL5 [465], CCL3 [466], C6 [467], MSR1 [468], HGF (hepatocyte growth factor) [469], VEGFA (vascular endothelial growth factor A) [470], ADM (adrenomedullin) [471], CR2 [472], MAG (myelin associated glycoprotein) [473], CDH1 [474], OLIG2 [475], SEMA4D [476], ADAMTS4 [477], BMP2 [478], ERBB3 [479] and NKX2-2 [480] have been identified as a hub gene in spinal cord injury in several studies.…”

Section: Discussionmentioning

confidence: 99%

“…FASLG (Fas ligand) [574], GJC2 [575] and GJB1 [576] have been identified to be involved in the development of spasticity. CD24 [577], CD28 [578], HLA-DRB5 [579], LTF (lactotransferrin) [580], GPNMB (glycoprotein nmb) [581], TNFRSF9 [582], LRRC37A2 [583], DRD3 [584], CD163 [369], HGF (hepatocyte growth factor) [585], TRPM8 [446], TTR (transthyretin) [586], VEGFA (vascular endothelial growth factor A) [587], CHI3L1 [588], MAG (myelin associated glycoprotein) [589], SREBF1 [217], HIP1R [590], HK2 [591], GPR37 [592], NGFR (nerve growth factor receptor) [593], TF (transferrin) [594], HAPLN2 [451], MOG (myelin oligodendrocyte glycoprotein) [595], BIN1 [596], BMP2 [597], GADD45B [598], UNC5B [599], ADORA1 [600], SEPTIN4 [601], DHCR7 [602], SCD (stearoyl-CoA desaturase) [603], GIPC1 [604], ALDH1A1 [605] and CTNNA3 [606] participate in pathogenic processes of Parkinson’s disease. At present, investigation on these key regulatory genes and related molecular pathways is lacking.…”

Section: Discussionmentioning

confidence: 99%

“…MOG (myelin oligodendrocyte glycoprotein) [431], ERBB3 [432], NHLH2 [433], GADD45B [434], PADI2 [435], ADORA1 [436], NINJ2 [437], WNT7A [438], DAO (D-amino acid oxidase) [439], PRODH (proline dehydrogenase 1) [440] and HCRTR1 [441] could regulate the development of psychiatric disorders. CCR2 [442], FASLG (Fas ligand) [443], GPNMB (glycoprotein nmb) [444], NPY2R [445], TRPM8 [446], TTR (transthyretin) [447], ADM (adrenomedullin) [448], CHI3L1 [375], CDH1 [377], HIP1R [449], SEMA4D [450], HAPLN2 [451], MYRF (myelin regulatory factor) [452], BIN1 [453] [464], CCL5 [465], CCL3 [466], C6 [467], MSR1 [468], HGF (hepatocyte growth factor) [469], VEGFA (vascular endothelial growth factor A) [470], ADM (adrenomedullin) [471], CR2 [472], MAG (myelin associated glycoprotein) [473], CDH1 [474], OLIG2 [475], SEMA4D [476], ADAMTS4 [477], BMP2 [478], ERBB3 [479] [488], CTLA4 [489], IRF4 [490], CHIT1 [491], NPY2R [492], TAB2 [131], CD52 [302], CD163 [493], MSR1 [306], HGF (hepatocyte growth factor) [494], TRPM8 [495], TTR (transthyretin) [496], F13A1 [497], ADM (adrenomedullin) …”

Section: Construction Of the Tf-hub Gene Regulatory Networkmentioning

confidence: 99%

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Identification of candidate biomarkers and pathways associated with multiple sclerosis using bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2023

Preprint

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Multiple sclerosis (MS) is the main reason for disability caused by autoimmunity. However, effective biomarkers for MS have not been identified. This study explored the molecular mechanisms and potential therapeutic targets for MS occurrence and progression using bioinformatics and next generation sequencing (NGS) data analysis. NGS data GSE138614, including patients with MS and 25 normal control samples, were obtained from Gene Expression Omnibus (GEO) database Differentially expressed genes (DEGs) were filtered and subjected to gene ontology (GO) and pathway enrichment analyses. Protein–protein interaction (PPI) network and module analyses were performed based on the DEGs. MiRNA-hub gene regulatory network and TF-hub gene regulatory network analysis were built by Cytoscape to predict the underlying microRNAs (miRNAs) and transcription factors (TFs) associated with hub genes. We also validated the identified hub genes via receiver operating characteristic (ROC) curve analysis. A total of 959 DEGs (479 up regulated genes and 480 down regulated genes) were detected. The GO terms and pathways of DEGs involve immune system process, developmental process, immune system and regulation of cholesterol biosynthesis by SREBP (SREBF). The network analysis revealed that hub genes include LCK, PYHIN1, SLAMF1, DOK2, TAB2, CFTR, RHOB, LMNA, EGLN3 and ERBB3 might be involved in the development of MS. The present investigation illustrates a characteristic gene profile in MS, which might contribute to the interpretation of the progression of MS and provide novel biomarkers and therapeutic targets for MS.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…MOG (myelin oligodendrocyte glycoprotein) [431], ERBB3 [432], NHLH2 [433], GADD45B [434], PADI2 [435], ADORA1 [436], NINJ2 [437], WNT7A [438], DAO (D-amino acid oxidase) [439], PRODH (proline dehydrogenase 1) [440] and HCRTR1 [441] could regulate the development of psychiatric disorders. CCR2 [442], FASLG (Fas ligand) [443], GPNMB (glycoprotein nmb) [444], NPY2R [445], TRPM8 [446], TTR (transthyretin) [447], ADM (adrenomedullin) [448], CHI3L1 [375], CDH1 [377], HIP1R [449], SEMA4D [450], HAPLN2 [451], MYRF (myelin regulatory factor) [452], BIN1 [453] [464], CCL5 [465], CCL3 [466], C6 [467], MSR1 [468], HGF (hepatocyte growth factor) [469], VEGFA (vascular endothelial growth factor A) [470], ADM (adrenomedullin) [471], CR2 [472], MAG (myelin associated glycoprotein) [473], CDH1 [474], OLIG2 [475], SEMA4D [476], ADAMTS4 [477], BMP2 [478], ERBB3 [479] [488], CTLA4 [489], IRF4 [490], CHIT1 [491], NPY2R [492], TAB2 [131], CD52 [302], CD163 [493], MSR1 [306], HGF (hepatocyte growth factor) [494], TRPM8 [495], TTR (transthyretin) [496], F13A1 [497], ADM (adrenomedullin) …”

Section: Construction Of the Tf-hub Gene Regulatory Networkmentioning

confidence: 99%

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Identification of candidate biomarkers and pathways associated with multiple sclerosis using bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2023

Preprint

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“…(2) stimulation of Ca 2+ permeable cation channels; and (3) the induction of apoptosis and cancer cell death via the stimulation of active caspase-3 (CASP3), -8 (CASP8), and -9 (CASP9) (Öz & Çelik, 2023;Xu et al, 2020). The transient receptor potential (TRP) is a superfamily of Ca 2+ permeable cation channels.…”

Section: Cell Ell B Biology Iology I International Nternationalmentioning

confidence: 99%

Silver nanoparticles stimulate 5‐Fluorouracil‐induced colorectal cancer cells to kill through the upregulation TRPV1‐mediated calcium signaling pathways

Kaya

2024

Cell Biology International

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The involvement of the TRP vanilloid 1 (TRPV1) cation channel on the 5‐Fluorouracil (5‐FU)‐caused Ca2+ signals through the activation of the apoptotic signaling pathway and stimulating the mitochondrial Ca2+ and Zn2+ accumulation‐induced reactive oxygen species (ROS) productions in several cancer cells, except the colorectal cancer (HT‐29) cell line, was recently reported. I aimed to investigate the action of silver nanoparticles (SiNPs) and 5‐FU incubations through the activation of TRPV1 on ROS, apoptosis, and cell death in the HT‐29 cell line. The cells were divided into four groups: control, SiNP (100 µM for 48 h), 5‐FU (25 μM for 24 h), and 5‐FU + SiNP. SiNP treatment through TRPV1 activation (via capsaicin) stimulated the oxidant and apoptotic actions of 5‐FU in the cells, whereas they were diminished in the cells by the TRPV1 antagonist (capsazepine) treatment. The apoptotic and cell death actions of 5‐FU were determined by increasing the propidium iodide/Hoechst rate, caspase‐3, ‐8, and ‐9 activations, mitochondrial membrane depolarization, lipid peroxidation, and ROS, but decreasing the glutathione and glutathione peroxidase. The increase of cytosolic free Ca2+ and Zn2+ into mitochondria via the stimulation of TRPV1 current density increased oxidant and apoptotic properties of 5‐FU in the cells. For the therapy of HT‐29 tumor cells, I found that the combination of SiNPs and 5‐FU was synergistic via TRPV1 activation.

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Erucic acid increases the potency of cisplatin‐induced colorectal cancer cell death and oxidative stress by upregulating the TRPM2 channel

Nazıroğlu,

Çarhan,

Nazıroğlu

2024

Cell Biology International

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Erucic acid (ErA) is a source of omega‐9 monounsaturated fatty acids. ErA exhibited antitumor effects by causing apoptosis and oxidative stress in tumor cells, with the exception of the HT‐29 human colorectal cancer cell line. The apoptotic and Ca2+ signaling pathways in tumor cells are triggered when mitochondrial Ca2+ and Zn2+ accumulation produce reactive free oxygen species (ROS), which in turn activate TRPM2. ErA‐induced ROS and TRPM2 stimulation may augment the anticancer action of cisplatin (CSP). We aimed to study the effects of ErA and CSP incubations on ROS, apoptosis, and cell death in the HT‐29 cells by activating TRPM2. The cells were divided into five groups: control, ErA (200 µM for 48 h), CSP (25 µM for 24 h), and ErA + CSP + TRPM2 antagonists (200 µM carvacrol and 25 µM N‐(p‐amylcinnamoyl)anthranilic acid for 24 h). The TRPM2 antagonists reduced ErA plus CSP‐induced increases in H2O2‐induced intracellular free Ca2+ concentration ([Ca2+]c) and adenosine diphosphate‐ribose‐caused TRPM2 currents. ErA and CSP were found to cause apoptosis and cell death by raising the intracellular free Zn2+ concentration (Zn2+]c), caspase‐3, −8, and −9, mitochondrial membrane dysfunction, and ROS, while lowering reduced glutathione, cell viability, and cell number. The oxidative, apoptotic, and tumor cell death effects of CSP in the cells were enhanced by the increase of ErA‐mediated [Ca2+]c and Zn2+]c entering mitochondria through the activation of TRPM2. In conclusion, we observed that the combination of ErA and CSP was synergistic via TRPM2 activation for the treatment of HT‐29 tumor cells.

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Downregulation of TRPM7, TRPM8, and TRPV1 channels modulate apoptotic parameters and neurodegenerative markers: Focus on neuronal differentiation and Parkinson's disease model

Cited by 6 publications

References 57 publications

Identification of candidate biomarkers and pathways associated with multiple sclerosis using bioinformatics and next generation sequencing data analysis

Identification of candidate biomarkers and pathways associated with multiple sclerosis using bioinformatics and next generation sequencing data analysis

Silver nanoparticles stimulate 5‐Fluorouracil‐induced colorectal cancer cells to kill through the upregulation TRPV1‐mediated calcium signaling pathways

Erucic acid increases the potency of cisplatin‐induced colorectal cancer cell death and oxidative stress by upregulating the TRPM2 channel

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