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1. Muscle-Restricted Nicotinamide Adenine Dinucleotide Phosphate Oxidase 4 Knockout Partially Corrects Muscle Contractility After Spinal Cord Injury in Mice

Author

Toro, Carlos A., primary, De Gasperi, Rita, additional, Aslan, Abdurrahman, additional, Johnson, Nicholas, additional, Siddiq, Mustafa M., additional, Chow, Christine, additional, Zhao, Wei, additional, Harlow, Lauren, additional, Graham, Zachary, additional, Liu, Xin-Hua, additional, Sadoshima, Junichi, additional, Iyengar, Ravi, additional, and Cardozo, Christopher P., additional

Published
2024
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2. Muscle-restricted Nox4 knockout partially corrects muscle contractility following spinal cord injury in mice

Author

Toro, Carlos A., primary, De Gasperi, Rita, additional, Aslan, Abdurrahman, additional, Johnson, Nicholas, additional, Siddiq, Mustafa M., additional, Chow, Christine, additional, Zhao, Wei, additional, Harlow, Lauren, additional, Graham, Zachary, additional, Liu, Xin-Hua, additional, Sadoshima, Junichi, additional, Iyengar, Ravi, additional, and Cardozo, Christopher P, additional

Published
2023
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5. Spinal Cord Injury regulates circular RNA expression in axons

Author

Siddiq, Mustafa M, primary, Toro, Carlos A, additional, Johnson, Nicholas P, additional, Hansen, Jens, additional, Xiong, Yuguang, additional, Mellado, Wilfredo, additional, Tolentino, Rosa E, additional, Johnson, Kaitlin, additional, Jayaraman, Gomathi, additional, Suhail, Zaara, additional, Harlow, Lauren, additional, Beaumont, Kristin G, additional, Sebra, Robert G, additional, Willis, Dianna E, additional, Cardozo, Christopher P, additional, and Iyengar, Ravi, additional

Published
2023
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6. Spinal cord injury regulates circular RNA expression in axons.

Author

Siddiq, Mustafa M., Toro, Carlos A., Johnson, Nicholas P., Hansen, Jens, Yuguang Xiong, Mellado, Wilfredo, Tolentino, Rosa E., Johnson, Kaitlin, Jayaraman, Gomathi, Suhail, Zaara, Harlow, Lauren, Jinye Dai, Beaumont, Kristin G., Sebra, Robert, Willis, Dianna E., Cardozo, Christopher P., and Iyengar, Ravi

Subjects
GENE expression, CIRCULAR RNA, SPINAL cord injuries, CATALYTIC RNA, NERVOUS system regeneration, RNA editing
Abstract

Introduction: Neurons transport mRNA and translational machinery to axons for local translation. After spinal cord injury (SCI), de novo translation is assumed to enable neurorepair. Knowledge of the identity of axonal mRNAs that participate in neurorepair after SCI is limited. We sought to identify and understand how axonal RNAs play a role in axonal regeneration. Methods: We obtained preparations enriched in axonal mRNAs from control and SCI rats by digesting spinal cord tissue with cold-active protease (CAP). The digested samples were then centrifuged to obtain a supernatant that was used to identify mRNA expression. We identified differentially expressed genes (DEGS) after SCI and mapped them to various biological processes. We validated the DEGs by RT-qPCR and RNA-scope. Results: The supernatant fraction was highly enriched for mRNA from axons. Using Gene Ontology, the second most significant pathway for all DEGs was axonogenesis. Among the DEGs was Rims2, which is predominately a circular RNA (circRNA) in the CNS. We show that Rims2 RNA within spinal cord axons is circular. We found an additional 200 putative circRNAs in the axonal-enriched fraction. Knockdown in primary rat cortical neurons of the RNA editing enzyme ADAR1, which inhibits formation of circRNAs, significantly increased axonal outgrowth and increased the expression of circRims2. Using Rims2 as a prototype we used Circular RNA Interactome to predict miRNAs that bind to circRims2 also bind to the 3'UTR of GAP-43, PTEN or CREB1, all known regulators of axonal outgrowth. Axonally-translated GAP-43 supports axonal elongation and we detect GAP-43 mRNA in the rat axons by RNAscope. Discussion: By enriching for axonal RNA, we detect SCI induced DEGs, including circRNA such as Rims2. Ablation of ADAR1, the enzyme that regulates circRNA formation, promotes axonal outgrowth of cortical neurons. We developed a pathway model using Circular RNA Interactome that indicates that Rims2 through miRNAs can regulate the axonal translation GAP-43 to regulate axonal regeneration. We conclude that axonal regulatory pathways will play a role in neurorepair. [ABSTRACT FROM AUTHOR]

Published
2023
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13. Numb is required for optimal contraction of skeletal muscle

Author

De Gasperi, Rita, primary, Mo, Chenglin, additional, Azulai, Daniella, additional, Wang, Zhiying, additional, Harlow, Lauren M., additional, Du, Yating, additional, Graham, Zachary, additional, Pan, Jiangping, additional, Liu, Xin‐hua, additional, Guo, Lei, additional, Zhang, Bin, additional, Ko, Fred, additional, Raczkowski, Ashleigh M., additional, Bauman, William A., additional, Goulbourne, Chris N., additional, Zhao, Wei, additional, Brotto, Marco, additional, and Cardozo, Christopher P., additional

Published
2022
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16. Numb is required for optimal contraction of skeletal muscle

Author

De Gasperi, Rita, primary, Mo, Chenglin, additional, Azulai, Daniella, additional, Wang, Zhiying, additional, Harlow, Lauren M., additional, Du, Yating, additional, Graham, Zachary, additional, Pan, Jiangping, additional, Liu, Xin-hua, additional, Guo, Lei, additional, Zhang, Bin, additional, Ko, Fred, additional, Raczkowski, Ashleigh M, additional, Bauman, William A., additional, Goulbourne, Chris N, additional, Zhao, Wei, additional, Brotto, Marco, additional, and Cardozo, Christopher P., additional

Published
2021
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20. Effects of a High-Fat Diet on Tissue Mass, Bone, and Glucose Tolerance after Chronic Complete Spinal Cord Transection in Male Mice

Author

Graham, Zachary A., primary, Liu, Xin-hua, additional, Harlow, Lauren, additional, Pan, Jiangping, additional, Azulai, Daniella, additional, Tawfeek, Hesham A., additional, Wnek, Russell D., additional, Mattingly, Alex J., additional, Bauman, William A., additional, Yarrow, Joshua F., additional, and Cardozo, Christopher P., additional

Published
2020
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26. Transcriptomic and growth responses to programmed resistance training in mouse, rat and human.

Author

Jarvis, Jonathan C., Viggars, Mark, Sutherland, Hazel, Harlow, Lauren, and Cardozo, Christopher

Subjects
RESISTANCE training, TRANSCRIPTOMES, GENE expression, RATS, MICE
Abstract

Mice are commonly used to investigate muscle biology and disease, but many labs have found it difficult to produce whole muscle hypertrophy without chronic overload or very long periods of training. We have established a model of muscle growth in the rat using programmed contractions in which the plantar flexors are used to resist the dorsiflexors of the ankle [1, 2]. We will present data from experiments in the rat that show a marked increase of muscle mass, showing how the acute transcriptomic response 1 hour after an exercise session changes as a muscle adapts to daily exercise over 30 days. We will also show that a similar degree of hypertrophy is achieved after 30 days with exercise every three days, and that the transcriptomic response in this case shows less change towards an 'endurance' expression profile. We will also present evidence from experiments using the same approach in mice, comparing the transcriptomic response of mouse muscle and rat muscle to the same protocol. In mice we see similar changes in gene expression but no increase in muscle mass. Future comparison of the transcriptomic and protein synthetic and degradative mechanisms in these models will be informative. [ABSTRACT FROM AUTHOR]

Published
2023
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28. Sclerostin Antibody Preserves the Morphology and Structure of Osteocytes and Blocks the Severe Skeletal Deterioration After Motor-Complete Spinal Cord Injury in Rats

Author

Qin, Weiping, primary, Li, Xiaodong, additional, Peng, Yuanzhen, additional, Harlow, Lauren M, additional, Ren, Yinshi, additional, Wu, Yingjie, additional, Li, Jiliang, additional, Qin, Yiwen, additional, Sun, Jie, additional, Zheng, Shijia, additional, Brown, Tom, additional, Feng, Jian Q, additional, Ke, Hua Zhu, additional, Bauman, William A, additional, and Cardozo, Christopher P, additional

Published
2016
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30. Sclerostin Antibody Preserves the Morphology and Structure of Osteocytes and Blocks the Severe Skeletal Deterioration After Motor-Complete Spinal Cord Injury in Rats

Author

Qin, Weiping, primary, Li, Xiaodong, additional, Peng, Yuanzhen, additional, Harlow, Lauren M, additional, Ren, Yinshi, additional, Wu, Yingjie, additional, Li, Jiliang, additional, Qin, Yiwen, additional, Sun, Jie, additional, Zheng, Shijia, additional, Brown, Tom, additional, Feng, Jian Q, additional, Ke, Hua Zhu, additional, Bauman, William A, additional, and Cardozo, Christopher C, additional

Published
2015
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31. Assessing the impact of boldine on the gastrocnemius using multiomics profiling at 7 and 28 days post-complete spinal cord injury in young male mice.

Author

Potter, Luke A., Toro, Carlos A., Harlow, Lauren, Lavin, Kaleen M., Cardozo, Christopher P., Wende, Adam R., and Graham, Zachary A.

Subjects
*SPINAL cord injuries, *MULTIOMICS, *SMALL molecules, *LEUCINE, *MUSCLE mass, *MUSCULAR atrophy
Abstract

Spinal cord injury (SCI) results in rapid muscle loss. Exogenous molecular interventions to slow muscle atrophy after SCI have been relatively ineffective and require the search for novel therapeutic targets. Connexin hemichannels (CxHCs) allow nonselective passage of small molecules into and out of the cell. Boldine, a CxHC-inhibiting aporphine found in the boldo tree (Peumus boldus), has shown promising preclinical results in slowing atrophy during sepsis and restoring muscle function in dysferlinopathy. We administered 50 mg/kg/day of boldine to spinal cord transected mice beginning 3 days post-injury. Tissue was collected 7 and 28 days post-SCI and the gastrocnemius was used for multiomics profiling. Boldine did not prevent body or muscle mass loss but attenuated SCI-induced changes in the abundance of the amino acids proline, phenylalanine, leucine and isoleucine, as well as glucose, 7 days post-SCI. SCI resulted in the differential expression of 7,700 and 2,000 genes at 7 and 28 days, respectively, compared with Sham controls. Pathway enrichment of these genes highlighted ribosome biogenesis at 7 days and translation and oxidative phosphorylation at both timepoints. Boldine altered the expression of 150 genes at 7 days and 110 genes at 28 days post-SCI. Pathway enrichment of these genes indicated a potential role for boldine in suppressing protein ubiquitination and degradation at the 7-day timepoint. Methylation analyses showed minimal differences between groups. Taken together, boldine is not an efficacious therapy to preserve body and muscle mass after complete SCI, though it attenuated some SCI-induced changes across the metabolome and transcriptome. [ABSTRACT FROM AUTHOR]

Published
2023
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35. Effects of a Laparotomy on Targeted Lipidomics Profiles in a Mouse Model of Surgical Stress During Aging.

Author

Huang J, Awad K, Harlow L, Toro CA, Brotto M, and Cardozo CP

Subjects
Animals, Mice, Chromatography, Liquid methods, Stress, Physiological, Disease Models, Animal, Lipids analysis, Lipids blood, Lipid Metabolism, Lipidomics methods, Laparotomy, Tandem Mass Spectrometry methods, Aging metabolism
Abstract

Laparotomy (EL) is one of the most common procedures performed among surgical specialties. Previous research demonstrates that surgery is associated with an increased inflammatory response. Low psoas muscle mass and quality markers are associated with increased mortality rates after emergency laparotomy. Analysis of lipid mediators in serum and muscle by using liquid chromatography-mass spectrometry (LC-MS)-based lipidomics has proven to be a sensitive and precise technique. In this chapter, we describe an LC-MS/MS protocol for the profiling and quantification of signaling lipids formed from Eicosapentaenoic Acid (EPA) and Eicosatetranoic acid (ETA) by 5, 12, or 15 lipoxynases. This protocol has been developed for and validated in serum and muscle samples in a mouse model of surgical stress caused by laparotomy., (© 2024. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

Published
2024
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36. Muscle-restricted Nox4 knockout partially corrects muscle contractility following spinal cord injury in mice.

Author

Toro CA, De Gasperi R, Aslan A, Johnson N, Siddiq MM, Chow C, Zhao W, Harlow L, Graham Z, Liu XH, Sadoshima J, Iyengar R, and Cardozo CP

Abstract

Spinal cord injury (SCI) results in severe atrophy of skeletal muscle in paralyzed regions, and a decrease in the force generated by muscle per unit of cross-sectional area. Oxidation of skeletal muscle ryanodine 1 receptors (RyR1) reduces contractile force due to reduced binding of calstabin 1 to RyR1 together with altered gating of RyR1. One cause of RyR1 oxidation is NADPH oxidase 4 (Nox4). We have previously shown that in rats, RyR1 was oxidized and bound less calstabin 1 at 56 days after spinal cord injury (SCI) by transection. Here, we used a conditional knock-out mouse model of Nox4 in muscle to investigate the role of Nox4 in reduced muscle specific force after SCI. Peak twitch force in control mice after SCI was reduced by 42% compared to sham-operated controls but was increased by approximately 43% in SCI Nox4 conditional KO mice compared to SCI controls although it remained less than that for sham-operated controls. Unlike what observed in rats, after SCI the expression of Nox4 was not increased in gastrocnemius muscle and binding of calstabin 1 to RyR1 was not reduced in this muscle. The results suggest a link between Nox4 expression in muscle tissue and reduction in muscle twitch force, however further studies are needed to understand the mechanistic basis for this linkage.

Published
2023
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