The Experts below are selected from a list of 93 Experts worldwide ranked by ideXlab platform
Srdjan M Vlajkovic - One of the best experts on this subject based on the ideXlab platform.
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Post exposure administration of A1 adenosine receptor agonists attenuates Noise-induced hearing loss
Hearing Research, 2010Co-Authors: Ann Chi Yan Wong, Rita Gupta, Gary D Housley, Peter R Thorne, Srdjan M VlajkovicAbstract:Abstract Adenosine is a constitutive cell metabolite with a putative role in protection and regeneration in many tissues. This study was undertaken to determine if adenosine signalling pathways are involved in protection against Noise Injury. A1 adenosine receptor expression levels were altered in the cochlea exposed to loud sound, suggesting their involvement in the development of Noise Injury. Adenosine and selective adenosine receptor agonists (CCPA, CGS-21680 and Cl-IB-MECA) were applied to the round window membrane of the cochlea 6 h after Noise exposure. Auditory brainstem responses measured 48 h after drug administration demonstrated partial recovery of hearing thresholds (up to 20 dB) in the cochleae treated with adenosine (non-selective adenosine receptor agonist) or CCPA (selective A1 adenosine receptor agonist). In contrast, the selective A2A adenosine receptor agonist CGS-21680 and A3 adenosine receptor agonist Cl-IB-MECA did not protect the cochlea from hearing loss. Sound-evoked cochlear potentials in control rats exposed to ambient Noise were minimally altered by local administration of the adenosine receptor agonists used in the Noise study. Free radical generation in the cochlea exposed to Noise was reduced by administration of adenosine and CCPA. This study pinpoints A1 adenosine receptors as attractive targets for pharmacological interventions to reduce Noise-induced cochlear Injury after exposure.
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Post exposure administration of A(1) adenosine receptor agonists attenuates Noise-induced hearing loss.
Hearing research, 2009Co-Authors: Ann Chi Yan Wong, Rita Gupta, Gary D Housley, Peter R Thorne, Srdjan M VlajkovicAbstract:Adenosine is a constitutive cell metabolite with a putative role in protection and regeneration in many tissues. This study was undertaken to determine if adenosine signalling pathways are involved in protection against Noise Injury. A(1) adenosine receptor expression levels were altered in the cochlea exposed to loud sound, suggesting their involvement in the development of Noise Injury. Adenosine and selective adenosine receptor agonists (CCPA, CGS-21680 and Cl-IB-MECA) were applied to the round window membrane of the cochlea 6h after Noise exposure. Auditory brainstem responses measured 48h after drug administration demonstrated partial recovery of hearing thresholds (up to 20dB) in the cochleae treated with adenosine (non-selective adenosine receptor agonist) or CCPA (selective A(1) adenosine receptor agonist). In contrast, the selective A(2A) adenosine receptor agonist CGS-21680 and A(3) adenosine receptor agonist Cl-IB-MECA did not protect the cochlea from hearing loss. Sound-evoked cochlear potentials in control rats exposed to ambient Noise were minimally altered by local administration of the adenosine receptor agonists used in the Noise study. Free radical generation in the cochlea exposed to Noise was reduced by administration of adenosine and CCPA. This study pinpoints A(1) adenosine receptors as attractive targets for pharmacological interventions to reduce Noise-induced cochlear Injury after exposure.
Teresa Partearroyo - One of the best experts on this subject based on the ideXlab platform.
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betaine homocysteine s methyltransferase deficiency causes increased susceptibility to Noise induced hearing loss associated with plasma hyperhomocysteinemia
The FASEB Journal, 2019Co-Authors: Teresa Partearroyo, Silvia Murillocuesta, Nestor Vallecillo, Jose Ma Bermudezmunoz, Lourdes Rodriguezde La Rosa, Giacomo MandruzzatoAbstract:Betaine-homocysteine S-methyltransferases (BHMTs) are methionine cycle enzymes that remethylate homocysteine; hence, their malfunction leads to hyperhomocysteinemia. Epidemiologic and experimental studies have revealed a correlation between hyperhomocysteinemia and hearing loss. Here, we have studied the expression of methionine cycle genes in the mouse cochlea and the impact of knocking out the Bhmt gene in the auditory receptor. We evaluated age-related changes in mouse hearing by recording auditory brainstem responses before and following exposure to Noise. Also, we measured cochlear cytoarchitecture, gene expression by RNA-arrays and quantitative RT-PCR, and metabolite levels in liver and plasma by HPLC. Our results indicate that there is an age-dependent strain-specific expression of methionine cycle genes in the mouse cochlea and a further regulation during the response to Noise damage. Loss of Bhmt did not cause an evident impact in the hearing acuity of young mice, but it produced higher threshold shifts and poorer recovery following Noise challenge. Hearing loss was associated with increased cochlear Injury, outer hair cell loss, altered expression of cochlear methionine cycle genes, and hyperhomocysteinemia. Our results suggest that BHMT plays a central role in the homeostasis of cochlear methionine metabolism and that Bhmt2 up-regulation could carry out a compensatory role in cochlear protection against Noise Injury in the absence of BHMT.-Partearroyo, T., Murillo-Cuesta, S., Vallecillo, N., Bermudez-Munoz, J. M., Rodriguez-de la Rosa, L., Mandruzzato, G., Celaya, A. M., Zeisel, S. H., Pajares, M. A., Varela-Moreiras, G., Varela-Nieto, I. Betaine-homocysteine S-methyltransferase deficiency causes increased susceptibility to Noise-induced hearing loss associated with plasma hyperhomocysteinemia.
Varela-moreiras Gregorio - One of the best experts on this subject based on the ideXlab platform.
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Betaine homocysteine s-methyltransferase deficiency increases susceptibility to Noise-induced hearing loss correlating with plasma hyperhomocysteinemia
2019Co-Authors: Partearroyo Teresa, Murillo-cuesta Silvia, Rodriguez-de La Rosa, Lourdes, Zeisel, Steven H., Pajares, María A., Varela-moreiras Gregorio, Varela-nieto IsabelAbstract:Resumen del póster presentado a NUTRIMAD: "Nutrición comunitaria en el siglo XXI", celebrada en Madrid del 24 al 27 de octubre de 2018.[Background] According to the World Health Organization, the incidence of auditory disorders, especially Noise-induced hearing loss, isincreasing dramatically. Genetic and environmentalfactors are part of the multifactorial aetiology of hearing loss, but nutritional imbalance is an emerging contributor. Epidemiological and experimental studies have revealed a correlation between hearing loss and increased plasma homocysteine (Hcy) secondary to methionine cycle impairment. Betaine homocysteine S-methyltransferases (BHMTs) are responsible for the remethylation of Hcy, hence their malfunction leadsto hyperhomocysteinemia. [Aim] To study the cochlear expression of methionine cycle genes and the impact of Bhmt knockdown in the response to Noise Injury. [Materials and methods] Mouse hearing was evaluated at different ages by recording auditory brainstem responses (ABR) and following Noise exposure. Cochlear cytoarchitecture was evaluated by histology and immunohistochemistry, and gene expression by RNA-arrays and RT-qPCR. Plasma and hepatic metabolite levels were determined by HPLC. [Results] Expression ofmethionine cycle genesin themouse cochlea is age-regulated.No evidentimpactin hearing acuitywas observed by loss of Bhmt expression in youngmice.However,following Noise challenge, knockout mice showed increased threshold shifts and poorerrecoverywith time, compared towild typemice. This enhanced susceptibility to Noise damage associated with severe alterations in cochlear cytoarchitecture, altered expression of cochlear methionine cycle genes and hyperhomocysteinemia. [Conclusions] BHMT plays a central role in the homeostasis of cochlear methionine metabolism. Bhmt deficiency leads to an increased susceptibility to Noise-induced hearing loss.Peer Reviewe
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Betaine homocysteine S-methyltransferase deficiency causes increased susceptibility to Noise-induced hearing loss associated to plasma hyperhomocysteinemia
'Japanese Society of Applied Entomology & Zoology', 2019Co-Authors: Murillo-cuesta Silvia, Partearroyo Teresa, Rodriguez-de La Rosa, Lourdes, Zeisel, Steven H., Pajares, María A., Varela-moreiras Gregorio, Vallecillo Néstor, Celaya, Adelaida M., Mandruzzato Giacomo, Varela-nieto IsabelAbstract:Resumen del trabajo presentado al 42st Annual Association for Research in Otolaryngology (ARO) MidWinter Meeting, celebrado en Baltimore, Maryland (USA) del 9 al 13 de febrero de 2019.Nutritional imbalance is an emerging causative factor for deafness and several epidemiological and experimental studies have linked alterations in methionine metabolism caused by folic acid and/or vitamin B12 deficiencies with age-related, Noiseinduced or sudden hearing loss. Betaine homocysteine S-methyltransferases (BHMTs) are methionine cycle enzymes that remethylate homocysteine, hence their malfunction leads to hyperhomocysteinemia. Here, we have studied the expression of methionine cycle genes in the mouse cochlea and the impact of knocking out the Bhmt gene in the auditory receptor. We evaluated age-related changes in mouse hearing by recording auditory brainstem responses at different moments from embryonic to adult stages, and following exposure to Noise. Also we measured cochlear cytoarchitecture, gene expression by RNA-arrays and RT-qPCR, and metabolite levels in liver and plasma by HPLC. Our results indicate that there is an age-dependent strain-specific expression of methionine cycle genes in the mouse cochlea and a further regulation during the response to Noise damage. Loss of Bhmt did not cause an evident impact in the hearing acuity of young mice, but it produced higher threshold shifts and poorer recovery following Noise challenge. Hearing loss was associated with increased cochlear Injury, altered expression of cochlear methionine cycle genes and hyperhomocysteinemia. Our results suggest that BHMT plays a central role in the homeostasis of cochlear methionine metabolism and that Bhmt2 upregulation could carry out a compensatory role in cochlear protection against Noise Injury in the absence of BHMT.Work supported by the Spanish MINECO/FEDER SAF2017-86107-R grant to IVN, U.S. National Institutes of Health DK056350 to SZ, and CEU-Banco Santander precompetitive (MUSPB047) and consolidation (MBS18C12) project to TP.Peer Reviewe
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Betaine-homocysteine S-methyltransferase deficiency causes increased susceptibility to Noise-induced hearing loss associated to plasma hyperhomocysteinemia
'FASEB', 2019Co-Authors: Partearroyo Teresa, Murillo-cuesta Silvia, Rodriguez-de La Rosa, Lourdes, Zeisel, Steven H., Pajares, María A., Vallecillo Néstor, Celaya, Adelaida M., Mandruzzato Giacomo, Bermúdez-muñoz, Jose Mª, Varela-moreiras GregorioAbstract:Betaine-homocysteine S-methyltransferases (BHMTs) are methionine cycle enzymes that remethylate homocysteine; hence, their malfunction leads to hyperhomocysteinemia. Epidemiologic and experimental studies have revealed a correlation between hyperhomocysteinemia and hearing loss. Here, we have studied the expression of methionine cycle genes in the mouse cochlea and the impact of knocking out the Bhmt gene in the auditory receptor. We evaluated age-related changes in mouse hearing by recording auditory brainstem responses before and following exposure to Noise. Also, we measured cochlear cytoarchitecture, gene expression by RNA-arrays and quantitative RT-PCR, and metabolite levels in liver and plasma by HPLC. Our results indicate that there is an age-dependent strain-specific expression of methionine cycle genes in the mouse cochlea and a further regulation during the response to Noise damage. Loss of Bhmt did not cause an evident impact in the hearing acuity of young mice, but it produced higher threshold shifts and poorer recovery following Noise challenge. Hearing loss was associated with increased cochlear Injury, outer hair cell loss, altered expression of cochlear methionine cycle genes, and hyperhomocysteinemia. Our results suggest that BHMT plays a central role in the homeostasis of cochlear methionine metabolism and that Bhmt2 up-regulation could carry out a compensatory role in cochlear protection against Noise Injury in the absence of BHMT.—Partearroyo, T., Murillo-Cuesta, S., Vallecillo, N., Bermúdez-Muñoz, J. M., Rodríguez-de la Rosa, L., Mandruzzato, G., Celaya, A. M., Zeisel, S. H., Pajares, M. A., Varela-Moreiras, G., Varela-Nieto, I. Betaine-homocysteine S-methyltransferase deficiency causes increased susceptibility to Noise-induced hearing loss associated to plasma hyperhomocysteinemia.This work was supported by the Spanish Ministerio de Economía y Competitividad (MINECO)/ FEDER SAF2017-86107-R to I.V.-N., U.S. National Institutes of Health (NIH), National Institute of Diabetes and Digestive and Kidney Diseases (Grant DK056350 to S.H.Z.), CEU-Banco Santander precompetitive project (MUSPB047) and CEUBanco Santander consolidation project (MBS18C12) to T.P., and Puleva BioFoods (to I.V.-N., G.V.-M., and M.A.P.). G.M. was supported by TARGEAR (FP7 PEOPLE 2013 IAPP612261).Peer reviewe
Ann Chi Yan Wong - One of the best experts on this subject based on the ideXlab platform.
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Post exposure administration of A1 adenosine receptor agonists attenuates Noise-induced hearing loss
Hearing Research, 2010Co-Authors: Ann Chi Yan Wong, Rita Gupta, Gary D Housley, Peter R Thorne, Srdjan M VlajkovicAbstract:Abstract Adenosine is a constitutive cell metabolite with a putative role in protection and regeneration in many tissues. This study was undertaken to determine if adenosine signalling pathways are involved in protection against Noise Injury. A1 adenosine receptor expression levels were altered in the cochlea exposed to loud sound, suggesting their involvement in the development of Noise Injury. Adenosine and selective adenosine receptor agonists (CCPA, CGS-21680 and Cl-IB-MECA) were applied to the round window membrane of the cochlea 6 h after Noise exposure. Auditory brainstem responses measured 48 h after drug administration demonstrated partial recovery of hearing thresholds (up to 20 dB) in the cochleae treated with adenosine (non-selective adenosine receptor agonist) or CCPA (selective A1 adenosine receptor agonist). In contrast, the selective A2A adenosine receptor agonist CGS-21680 and A3 adenosine receptor agonist Cl-IB-MECA did not protect the cochlea from hearing loss. Sound-evoked cochlear potentials in control rats exposed to ambient Noise were minimally altered by local administration of the adenosine receptor agonists used in the Noise study. Free radical generation in the cochlea exposed to Noise was reduced by administration of adenosine and CCPA. This study pinpoints A1 adenosine receptors as attractive targets for pharmacological interventions to reduce Noise-induced cochlear Injury after exposure.
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Post exposure administration of A(1) adenosine receptor agonists attenuates Noise-induced hearing loss.
Hearing research, 2009Co-Authors: Ann Chi Yan Wong, Rita Gupta, Gary D Housley, Peter R Thorne, Srdjan M VlajkovicAbstract:Adenosine is a constitutive cell metabolite with a putative role in protection and regeneration in many tissues. This study was undertaken to determine if adenosine signalling pathways are involved in protection against Noise Injury. A(1) adenosine receptor expression levels were altered in the cochlea exposed to loud sound, suggesting their involvement in the development of Noise Injury. Adenosine and selective adenosine receptor agonists (CCPA, CGS-21680 and Cl-IB-MECA) were applied to the round window membrane of the cochlea 6h after Noise exposure. Auditory brainstem responses measured 48h after drug administration demonstrated partial recovery of hearing thresholds (up to 20dB) in the cochleae treated with adenosine (non-selective adenosine receptor agonist) or CCPA (selective A(1) adenosine receptor agonist). In contrast, the selective A(2A) adenosine receptor agonist CGS-21680 and A(3) adenosine receptor agonist Cl-IB-MECA did not protect the cochlea from hearing loss. Sound-evoked cochlear potentials in control rats exposed to ambient Noise were minimally altered by local administration of the adenosine receptor agonists used in the Noise study. Free radical generation in the cochlea exposed to Noise was reduced by administration of adenosine and CCPA. This study pinpoints A(1) adenosine receptors as attractive targets for pharmacological interventions to reduce Noise-induced cochlear Injury after exposure.
Giacomo Mandruzzato - One of the best experts on this subject based on the ideXlab platform.
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betaine homocysteine s methyltransferase deficiency causes increased susceptibility to Noise induced hearing loss associated with plasma hyperhomocysteinemia
The FASEB Journal, 2019Co-Authors: Teresa Partearroyo, Silvia Murillocuesta, Nestor Vallecillo, Jose Ma Bermudezmunoz, Lourdes Rodriguezde La Rosa, Giacomo MandruzzatoAbstract:Betaine-homocysteine S-methyltransferases (BHMTs) are methionine cycle enzymes that remethylate homocysteine; hence, their malfunction leads to hyperhomocysteinemia. Epidemiologic and experimental studies have revealed a correlation between hyperhomocysteinemia and hearing loss. Here, we have studied the expression of methionine cycle genes in the mouse cochlea and the impact of knocking out the Bhmt gene in the auditory receptor. We evaluated age-related changes in mouse hearing by recording auditory brainstem responses before and following exposure to Noise. Also, we measured cochlear cytoarchitecture, gene expression by RNA-arrays and quantitative RT-PCR, and metabolite levels in liver and plasma by HPLC. Our results indicate that there is an age-dependent strain-specific expression of methionine cycle genes in the mouse cochlea and a further regulation during the response to Noise damage. Loss of Bhmt did not cause an evident impact in the hearing acuity of young mice, but it produced higher threshold shifts and poorer recovery following Noise challenge. Hearing loss was associated with increased cochlear Injury, outer hair cell loss, altered expression of cochlear methionine cycle genes, and hyperhomocysteinemia. Our results suggest that BHMT plays a central role in the homeostasis of cochlear methionine metabolism and that Bhmt2 up-regulation could carry out a compensatory role in cochlear protection against Noise Injury in the absence of BHMT.-Partearroyo, T., Murillo-Cuesta, S., Vallecillo, N., Bermudez-Munoz, J. M., Rodriguez-de la Rosa, L., Mandruzzato, G., Celaya, A. M., Zeisel, S. H., Pajares, M. A., Varela-Moreiras, G., Varela-Nieto, I. Betaine-homocysteine S-methyltransferase deficiency causes increased susceptibility to Noise-induced hearing loss associated with plasma hyperhomocysteinemia.