Berberine coated mannosylated liposomes curtail RANKL stimulated osteoclastogenesis through the modulation of GSK3β pathway via upregulating miR-23a

Drug-induced microRNAs manifest significant therapeutic approaches; however, such progress in the treatment of osteopathic disorders including osteoporosis and rheumatoid arthritis still remains obscure. Contrarily, non-specific drug delivery, at high doses, increases the risk of side effects and re...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Sujitha, Sali [verfasserIn] Rasool, Mahaboobkhan [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	Rheumatoid arthritis ML-BBR miR-23a GSK3β/p-GSK3β Osteoclastogenesis

Übergeordnetes Werk:	Enthalten in: International immunopharmacology - Amsterdam [u.a.] : Elsevier Science, 2001, 74
Übergeordnetes Werk:	volume:74

DOI / URN:	10.1016/j.intimp.2019.105703

Katalog-ID:	ELV002763613

Internformat


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245	1	0	\|a Berberine coated mannosylated liposomes curtail RANKL stimulated osteoclastogenesis through the modulation of GSK3β pathway via upregulating miR-23a
264		1	\|c 2019
336			\|a nicht spezifiziert \|b zzz \|2 rdacontent
337			\|a Computermedien \|b c \|2 rdamedia
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520			\|a Drug-induced microRNAs manifest significant therapeutic approaches; however, such progress in the treatment of osteopathic disorders including osteoporosis and rheumatoid arthritis still remains obscure. Contrarily, non-specific drug delivery, at high doses, increases the risk of side effects and reduces drug therapeutic efficacy. Accordingly, the present study was designed to examine the therapeutic effect of berberine coated mannosylated liposomes (ML-BBR) on RANKL (100 ng/ml) stimulated bone marrow-derived monocytes/macrophages (BMMs) via altering miR-23a expression. Initial studies using confocal microscopy showed successful internalization of ML-BBR in RANKL stimulated BMMs. Treatment with ML-BBR abrogated the increased osteoclast formation in BMM cells via inhibiting phosphorylated glutathione synthase kinase beta (p-GSK3β) mediated NFATc1 activation. Consequently, ML-BBR also attenuated the expression of bone-degrading enzymes (TRAP, cathepsin K and MMP-9) thereby inhibiting the bone resorptive activity of osteoclasts. Moreover, ML-BBR induced the expression levels of miR-23a at the gene level, which in turn attenuated GSK3β/p-GSK3β expression as confirmed via blotting analysis. Further miR-23a inhibition of the GSK3β phosphorylation was confirmed using luciferase reporter assay. Comparatively, LY2090314 (GSK3β inhibitor) treatment inhibited the protein level expression of GSK3β/p-GSK3β. However, LY2090314 treatment induced a basal level expression of miR-23a owing to the suggestion that ML-BBR has an influential role in upregulating miR-23a level to inhibit GSK-3β phosphorylation. Cumulatively, our findings endorsed that preferential internalization of ML-BBR by BMMs effectively modulated the RANKL/p-GSK3β pathway and curtailed the osteoclast-mediated bone erosion possibly through post-transcriptional gene silencing via miR-23a.
650		4	\|a Rheumatoid arthritis
650		4	\|a ML-BBR
650		4	\|a miR-23a
650		4	\|a GSK3β/p-GSK3β
650		4	\|a Osteoclastogenesis
700	1		\|a Rasool, Mahaboobkhan \|e verfasserin \|4 aut
773	0	8	\|i Enthalten in \|t International immunopharmacology \|d Amsterdam [u.a.] : Elsevier Science, 2001 \|g 74 \|h Online-Ressource \|w (DE-627)330614630 \|w (DE-600)2049924-3 \|w (DE-576)259272272 \|x 1878-1705 \|7 nnns
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912			\|a GBV_ILN_2027
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912			\|a GBV_ILN_4335
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4393
936	b	k	\|a 44.38 \|j Pharmakologie
951			\|a AR
952			\|d 74

Indexfelder

author_variant	s s ss m r mr
matchkey_str	article:18781705:2019----::ebrncaemnoyaelpsmsutirnltmltdsecatgnsshogteouain
hierarchy_sort_str	2019
bklnumber	44.38
publishDate	2019
allfields	10.1016/j.intimp.2019.105703 doi (DE-627)ELV002763613 (ELSEVIER)S1567-5769(19)30913-0 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Sujitha, Sali verfasserin aut Berberine coated mannosylated liposomes curtail RANKL stimulated osteoclastogenesis through the modulation of GSK3β pathway via upregulating miR-23a 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Drug-induced microRNAs manifest significant therapeutic approaches; however, such progress in the treatment of osteopathic disorders including osteoporosis and rheumatoid arthritis still remains obscure. Contrarily, non-specific drug delivery, at high doses, increases the risk of side effects and reduces drug therapeutic efficacy. Accordingly, the present study was designed to examine the therapeutic effect of berberine coated mannosylated liposomes (ML-BBR) on RANKL (100 ng/ml) stimulated bone marrow-derived monocytes/macrophages (BMMs) via altering miR-23a expression. Initial studies using confocal microscopy showed successful internalization of ML-BBR in RANKL stimulated BMMs. Treatment with ML-BBR abrogated the increased osteoclast formation in BMM cells via inhibiting phosphorylated glutathione synthase kinase beta (p-GSK3β) mediated NFATc1 activation. Consequently, ML-BBR also attenuated the expression of bone-degrading enzymes (TRAP, cathepsin K and MMP-9) thereby inhibiting the bone resorptive activity of osteoclasts. Moreover, ML-BBR induced the expression levels of miR-23a at the gene level, which in turn attenuated GSK3β/p-GSK3β expression as confirmed via blotting analysis. Further miR-23a inhibition of the GSK3β phosphorylation was confirmed using luciferase reporter assay. Comparatively, LY2090314 (GSK3β inhibitor) treatment inhibited the protein level expression of GSK3β/p-GSK3β. However, LY2090314 treatment induced a basal level expression of miR-23a owing to the suggestion that ML-BBR has an influential role in upregulating miR-23a level to inhibit GSK-3β phosphorylation. Cumulatively, our findings endorsed that preferential internalization of ML-BBR by BMMs effectively modulated the RANKL/p-GSK3β pathway and curtailed the osteoclast-mediated bone erosion possibly through post-transcriptional gene silencing via miR-23a. Rheumatoid arthritis ML-BBR miR-23a GSK3β/p-GSK3β Osteoclastogenesis Rasool, Mahaboobkhan verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 74 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:74 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 74
spelling	10.1016/j.intimp.2019.105703 doi (DE-627)ELV002763613 (ELSEVIER)S1567-5769(19)30913-0 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Sujitha, Sali verfasserin aut Berberine coated mannosylated liposomes curtail RANKL stimulated osteoclastogenesis through the modulation of GSK3β pathway via upregulating miR-23a 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Drug-induced microRNAs manifest significant therapeutic approaches; however, such progress in the treatment of osteopathic disorders including osteoporosis and rheumatoid arthritis still remains obscure. Contrarily, non-specific drug delivery, at high doses, increases the risk of side effects and reduces drug therapeutic efficacy. Accordingly, the present study was designed to examine the therapeutic effect of berberine coated mannosylated liposomes (ML-BBR) on RANKL (100 ng/ml) stimulated bone marrow-derived monocytes/macrophages (BMMs) via altering miR-23a expression. Initial studies using confocal microscopy showed successful internalization of ML-BBR in RANKL stimulated BMMs. Treatment with ML-BBR abrogated the increased osteoclast formation in BMM cells via inhibiting phosphorylated glutathione synthase kinase beta (p-GSK3β) mediated NFATc1 activation. Consequently, ML-BBR also attenuated the expression of bone-degrading enzymes (TRAP, cathepsin K and MMP-9) thereby inhibiting the bone resorptive activity of osteoclasts. Moreover, ML-BBR induced the expression levels of miR-23a at the gene level, which in turn attenuated GSK3β/p-GSK3β expression as confirmed via blotting analysis. Further miR-23a inhibition of the GSK3β phosphorylation was confirmed using luciferase reporter assay. Comparatively, LY2090314 (GSK3β inhibitor) treatment inhibited the protein level expression of GSK3β/p-GSK3β. However, LY2090314 treatment induced a basal level expression of miR-23a owing to the suggestion that ML-BBR has an influential role in upregulating miR-23a level to inhibit GSK-3β phosphorylation. Cumulatively, our findings endorsed that preferential internalization of ML-BBR by BMMs effectively modulated the RANKL/p-GSK3β pathway and curtailed the osteoclast-mediated bone erosion possibly through post-transcriptional gene silencing via miR-23a. Rheumatoid arthritis ML-BBR miR-23a GSK3β/p-GSK3β Osteoclastogenesis Rasool, Mahaboobkhan verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 74 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:74 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 74
allfields_unstemmed	10.1016/j.intimp.2019.105703 doi (DE-627)ELV002763613 (ELSEVIER)S1567-5769(19)30913-0 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Sujitha, Sali verfasserin aut Berberine coated mannosylated liposomes curtail RANKL stimulated osteoclastogenesis through the modulation of GSK3β pathway via upregulating miR-23a 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Drug-induced microRNAs manifest significant therapeutic approaches; however, such progress in the treatment of osteopathic disorders including osteoporosis and rheumatoid arthritis still remains obscure. Contrarily, non-specific drug delivery, at high doses, increases the risk of side effects and reduces drug therapeutic efficacy. Accordingly, the present study was designed to examine the therapeutic effect of berberine coated mannosylated liposomes (ML-BBR) on RANKL (100 ng/ml) stimulated bone marrow-derived monocytes/macrophages (BMMs) via altering miR-23a expression. Initial studies using confocal microscopy showed successful internalization of ML-BBR in RANKL stimulated BMMs. Treatment with ML-BBR abrogated the increased osteoclast formation in BMM cells via inhibiting phosphorylated glutathione synthase kinase beta (p-GSK3β) mediated NFATc1 activation. Consequently, ML-BBR also attenuated the expression of bone-degrading enzymes (TRAP, cathepsin K and MMP-9) thereby inhibiting the bone resorptive activity of osteoclasts. Moreover, ML-BBR induced the expression levels of miR-23a at the gene level, which in turn attenuated GSK3β/p-GSK3β expression as confirmed via blotting analysis. Further miR-23a inhibition of the GSK3β phosphorylation was confirmed using luciferase reporter assay. Comparatively, LY2090314 (GSK3β inhibitor) treatment inhibited the protein level expression of GSK3β/p-GSK3β. However, LY2090314 treatment induced a basal level expression of miR-23a owing to the suggestion that ML-BBR has an influential role in upregulating miR-23a level to inhibit GSK-3β phosphorylation. Cumulatively, our findings endorsed that preferential internalization of ML-BBR by BMMs effectively modulated the RANKL/p-GSK3β pathway and curtailed the osteoclast-mediated bone erosion possibly through post-transcriptional gene silencing via miR-23a. Rheumatoid arthritis ML-BBR miR-23a GSK3β/p-GSK3β Osteoclastogenesis Rasool, Mahaboobkhan verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 74 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:74 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 74
allfieldsGer	10.1016/j.intimp.2019.105703 doi (DE-627)ELV002763613 (ELSEVIER)S1567-5769(19)30913-0 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Sujitha, Sali verfasserin aut Berberine coated mannosylated liposomes curtail RANKL stimulated osteoclastogenesis through the modulation of GSK3β pathway via upregulating miR-23a 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Drug-induced microRNAs manifest significant therapeutic approaches; however, such progress in the treatment of osteopathic disorders including osteoporosis and rheumatoid arthritis still remains obscure. Contrarily, non-specific drug delivery, at high doses, increases the risk of side effects and reduces drug therapeutic efficacy. Accordingly, the present study was designed to examine the therapeutic effect of berberine coated mannosylated liposomes (ML-BBR) on RANKL (100 ng/ml) stimulated bone marrow-derived monocytes/macrophages (BMMs) via altering miR-23a expression. Initial studies using confocal microscopy showed successful internalization of ML-BBR in RANKL stimulated BMMs. Treatment with ML-BBR abrogated the increased osteoclast formation in BMM cells via inhibiting phosphorylated glutathione synthase kinase beta (p-GSK3β) mediated NFATc1 activation. Consequently, ML-BBR also attenuated the expression of bone-degrading enzymes (TRAP, cathepsin K and MMP-9) thereby inhibiting the bone resorptive activity of osteoclasts. Moreover, ML-BBR induced the expression levels of miR-23a at the gene level, which in turn attenuated GSK3β/p-GSK3β expression as confirmed via blotting analysis. Further miR-23a inhibition of the GSK3β phosphorylation was confirmed using luciferase reporter assay. Comparatively, LY2090314 (GSK3β inhibitor) treatment inhibited the protein level expression of GSK3β/p-GSK3β. However, LY2090314 treatment induced a basal level expression of miR-23a owing to the suggestion that ML-BBR has an influential role in upregulating miR-23a level to inhibit GSK-3β phosphorylation. Cumulatively, our findings endorsed that preferential internalization of ML-BBR by BMMs effectively modulated the RANKL/p-GSK3β pathway and curtailed the osteoclast-mediated bone erosion possibly through post-transcriptional gene silencing via miR-23a. Rheumatoid arthritis ML-BBR miR-23a GSK3β/p-GSK3β Osteoclastogenesis Rasool, Mahaboobkhan verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 74 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:74 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 74
allfieldsSound	10.1016/j.intimp.2019.105703 doi (DE-627)ELV002763613 (ELSEVIER)S1567-5769(19)30913-0 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Sujitha, Sali verfasserin aut Berberine coated mannosylated liposomes curtail RANKL stimulated osteoclastogenesis through the modulation of GSK3β pathway via upregulating miR-23a 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Drug-induced microRNAs manifest significant therapeutic approaches; however, such progress in the treatment of osteopathic disorders including osteoporosis and rheumatoid arthritis still remains obscure. Contrarily, non-specific drug delivery, at high doses, increases the risk of side effects and reduces drug therapeutic efficacy. Accordingly, the present study was designed to examine the therapeutic effect of berberine coated mannosylated liposomes (ML-BBR) on RANKL (100 ng/ml) stimulated bone marrow-derived monocytes/macrophages (BMMs) via altering miR-23a expression. Initial studies using confocal microscopy showed successful internalization of ML-BBR in RANKL stimulated BMMs. Treatment with ML-BBR abrogated the increased osteoclast formation in BMM cells via inhibiting phosphorylated glutathione synthase kinase beta (p-GSK3β) mediated NFATc1 activation. Consequently, ML-BBR also attenuated the expression of bone-degrading enzymes (TRAP, cathepsin K and MMP-9) thereby inhibiting the bone resorptive activity of osteoclasts. Moreover, ML-BBR induced the expression levels of miR-23a at the gene level, which in turn attenuated GSK3β/p-GSK3β expression as confirmed via blotting analysis. Further miR-23a inhibition of the GSK3β phosphorylation was confirmed using luciferase reporter assay. Comparatively, LY2090314 (GSK3β inhibitor) treatment inhibited the protein level expression of GSK3β/p-GSK3β. However, LY2090314 treatment induced a basal level expression of miR-23a owing to the suggestion that ML-BBR has an influential role in upregulating miR-23a level to inhibit GSK-3β phosphorylation. Cumulatively, our findings endorsed that preferential internalization of ML-BBR by BMMs effectively modulated the RANKL/p-GSK3β pathway and curtailed the osteoclast-mediated bone erosion possibly through post-transcriptional gene silencing via miR-23a. Rheumatoid arthritis ML-BBR miR-23a GSK3β/p-GSK3β Osteoclastogenesis Rasool, Mahaboobkhan verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 74 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:74 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 74
language	English
source	Enthalten in International immunopharmacology 74 volume:74
sourceStr	Enthalten in International immunopharmacology 74 volume:74
format_phy_str_mv	Article
bklname	Pharmakologie
institution	findex.gbv.de
topic_facet	Rheumatoid arthritis ML-BBR miR-23a GSK3β/p-GSK3β Osteoclastogenesis
dewey-raw	610
isfreeaccess_bool	false
container_title	International immunopharmacology
authorswithroles_txt_mv	Sujitha, Sali @@aut@@ Rasool, Mahaboobkhan @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
hierarchy_top_id	330614630
dewey-sort	3610
id	ELV002763613
language_de	englisch
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author	Sujitha, Sali
spellingShingle	Sujitha, Sali ddc 610 fid PHARM bkl 44.38 misc Rheumatoid arthritis misc ML-BBR misc miR-23a misc GSK3β/p-GSK3β misc Osteoclastogenesis Berberine coated mannosylated liposomes curtail RANKL stimulated osteoclastogenesis through the modulation of GSK3β pathway via upregulating miR-23a
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topic_title	610 DE-600 PHARM DE-84 fid 44.38 bkl Berberine coated mannosylated liposomes curtail RANKL stimulated osteoclastogenesis through the modulation of GSK3β pathway via upregulating miR-23a Rheumatoid arthritis ML-BBR miR-23a GSK3β/p-GSK3β Osteoclastogenesis
topic	ddc 610 fid PHARM bkl 44.38 misc Rheumatoid arthritis misc ML-BBR misc miR-23a misc GSK3β/p-GSK3β misc Osteoclastogenesis
topic_unstemmed	ddc 610 fid PHARM bkl 44.38 misc Rheumatoid arthritis misc ML-BBR misc miR-23a misc GSK3β/p-GSK3β misc Osteoclastogenesis
topic_browse	ddc 610 fid PHARM bkl 44.38 misc Rheumatoid arthritis misc ML-BBR misc miR-23a misc GSK3β/p-GSK3β misc Osteoclastogenesis
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title	Berberine coated mannosylated liposomes curtail RANKL stimulated osteoclastogenesis through the modulation of GSK3β pathway via upregulating miR-23a
ctrlnum	(DE-627)ELV002763613 (ELSEVIER)S1567-5769(19)30913-0
title_full	Berberine coated mannosylated liposomes curtail RANKL stimulated osteoclastogenesis through the modulation of GSK3β pathway via upregulating miR-23a
author_sort	Sujitha, Sali
journal	International immunopharmacology
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author_browse	Sujitha, Sali Rasool, Mahaboobkhan
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author-letter	Sujitha, Sali
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title_sort	berberine coated mannosylated liposomes curtail rankl stimulated osteoclastogenesis through the modulation of gsk3β pathway via upregulating mir-23a
title_auth	Berberine coated mannosylated liposomes curtail RANKL stimulated osteoclastogenesis through the modulation of GSK3β pathway via upregulating miR-23a
abstract	Drug-induced microRNAs manifest significant therapeutic approaches; however, such progress in the treatment of osteopathic disorders including osteoporosis and rheumatoid arthritis still remains obscure. Contrarily, non-specific drug delivery, at high doses, increases the risk of side effects and reduces drug therapeutic efficacy. Accordingly, the present study was designed to examine the therapeutic effect of berberine coated mannosylated liposomes (ML-BBR) on RANKL (100 ng/ml) stimulated bone marrow-derived monocytes/macrophages (BMMs) via altering miR-23a expression. Initial studies using confocal microscopy showed successful internalization of ML-BBR in RANKL stimulated BMMs. Treatment with ML-BBR abrogated the increased osteoclast formation in BMM cells via inhibiting phosphorylated glutathione synthase kinase beta (p-GSK3β) mediated NFATc1 activation. Consequently, ML-BBR also attenuated the expression of bone-degrading enzymes (TRAP, cathepsin K and MMP-9) thereby inhibiting the bone resorptive activity of osteoclasts. Moreover, ML-BBR induced the expression levels of miR-23a at the gene level, which in turn attenuated GSK3β/p-GSK3β expression as confirmed via blotting analysis. Further miR-23a inhibition of the GSK3β phosphorylation was confirmed using luciferase reporter assay. Comparatively, LY2090314 (GSK3β inhibitor) treatment inhibited the protein level expression of GSK3β/p-GSK3β. However, LY2090314 treatment induced a basal level expression of miR-23a owing to the suggestion that ML-BBR has an influential role in upregulating miR-23a level to inhibit GSK-3β phosphorylation. Cumulatively, our findings endorsed that preferential internalization of ML-BBR by BMMs effectively modulated the RANKL/p-GSK3β pathway and curtailed the osteoclast-mediated bone erosion possibly through post-transcriptional gene silencing via miR-23a.
abstractGer	Drug-induced microRNAs manifest significant therapeutic approaches; however, such progress in the treatment of osteopathic disorders including osteoporosis and rheumatoid arthritis still remains obscure. Contrarily, non-specific drug delivery, at high doses, increases the risk of side effects and reduces drug therapeutic efficacy. Accordingly, the present study was designed to examine the therapeutic effect of berberine coated mannosylated liposomes (ML-BBR) on RANKL (100 ng/ml) stimulated bone marrow-derived monocytes/macrophages (BMMs) via altering miR-23a expression. Initial studies using confocal microscopy showed successful internalization of ML-BBR in RANKL stimulated BMMs. Treatment with ML-BBR abrogated the increased osteoclast formation in BMM cells via inhibiting phosphorylated glutathione synthase kinase beta (p-GSK3β) mediated NFATc1 activation. Consequently, ML-BBR also attenuated the expression of bone-degrading enzymes (TRAP, cathepsin K and MMP-9) thereby inhibiting the bone resorptive activity of osteoclasts. Moreover, ML-BBR induced the expression levels of miR-23a at the gene level, which in turn attenuated GSK3β/p-GSK3β expression as confirmed via blotting analysis. Further miR-23a inhibition of the GSK3β phosphorylation was confirmed using luciferase reporter assay. Comparatively, LY2090314 (GSK3β inhibitor) treatment inhibited the protein level expression of GSK3β/p-GSK3β. However, LY2090314 treatment induced a basal level expression of miR-23a owing to the suggestion that ML-BBR has an influential role in upregulating miR-23a level to inhibit GSK-3β phosphorylation. Cumulatively, our findings endorsed that preferential internalization of ML-BBR by BMMs effectively modulated the RANKL/p-GSK3β pathway and curtailed the osteoclast-mediated bone erosion possibly through post-transcriptional gene silencing via miR-23a.
abstract_unstemmed	Drug-induced microRNAs manifest significant therapeutic approaches; however, such progress in the treatment of osteopathic disorders including osteoporosis and rheumatoid arthritis still remains obscure. Contrarily, non-specific drug delivery, at high doses, increases the risk of side effects and reduces drug therapeutic efficacy. Accordingly, the present study was designed to examine the therapeutic effect of berberine coated mannosylated liposomes (ML-BBR) on RANKL (100 ng/ml) stimulated bone marrow-derived monocytes/macrophages (BMMs) via altering miR-23a expression. Initial studies using confocal microscopy showed successful internalization of ML-BBR in RANKL stimulated BMMs. Treatment with ML-BBR abrogated the increased osteoclast formation in BMM cells via inhibiting phosphorylated glutathione synthase kinase beta (p-GSK3β) mediated NFATc1 activation. Consequently, ML-BBR also attenuated the expression of bone-degrading enzymes (TRAP, cathepsin K and MMP-9) thereby inhibiting the bone resorptive activity of osteoclasts. Moreover, ML-BBR induced the expression levels of miR-23a at the gene level, which in turn attenuated GSK3β/p-GSK3β expression as confirmed via blotting analysis. Further miR-23a inhibition of the GSK3β phosphorylation was confirmed using luciferase reporter assay. Comparatively, LY2090314 (GSK3β inhibitor) treatment inhibited the protein level expression of GSK3β/p-GSK3β. However, LY2090314 treatment induced a basal level expression of miR-23a owing to the suggestion that ML-BBR has an influential role in upregulating miR-23a level to inhibit GSK-3β phosphorylation. Cumulatively, our findings endorsed that preferential internalization of ML-BBR by BMMs effectively modulated the RANKL/p-GSK3β pathway and curtailed the osteoclast-mediated bone erosion possibly through post-transcriptional gene silencing via miR-23a.
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title_short	Berberine coated mannosylated liposomes curtail RANKL stimulated osteoclastogenesis through the modulation of GSK3β pathway via upregulating miR-23a
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up_date	2024-07-06T17:22:14.301Z
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Berberine coated mannosylated liposomes curtail RANKL stimulated osteoclastogenesis through the modulation of GSK3β pathway via upregulating miR-23a

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