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Transcriptional changes in sensory ganglia associated with primary afferent axon collateral sprouting in spared dermatome model.

ABSTRACT: Primary afferent collateral sprouting is a process whereby non-injured primary afferent neurons respond to some stimulus and extend new branches from existing axons. Neurons of both the central and peripheral nervous systems undergo this process, which contributes to both adaptive and maladaptive plasticity (e.g., [1], [2], [3], [4], [5], [6], [7], [8], [9]). In the model used here (the "spared dermatome" model), the intact sensory neurons respond to the denervation of adjacent areas of skin by sprouting new axon branches into that adjacent denervated territory. Investigations of gene expression changes associated with collateral sprouting can provide a better understanding of the molecular mechanisms controlling this process. Consequently, it can be used to develop treatments to promote functional recovery for spinal cord injury and other similar conditions. This report includes raw gene expression data files from microarray experiments in order to study the gene regulation in spared sensory ganglia in the initiation (7 days) and maintenance (14 days) phases of the spared dermatome model relative to intact ("naïve") sensory ganglia. Data has been deposited into GEO (GSE72551).

SUBMITTER: Harrison BJ

PROVIDER: S-EPMC4664766 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature

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Transcriptional changes in sensory ganglia associated with primary afferent axon collateral sprouting in spared dermatome model.

Harrison Benjamin J BJ Venkat Gayathri G Hutson Thomas T Rau Kristofer K KK Bunge Mary Bartlett MB Mendell Lorne M LM Gage Fred H FH Johnson Richard D RD Hill Caitlin C Rouchka Eric C EC Moon Lawrence L Petruska Jeffrey C JC

Genomics data 20151023

Primary afferent collateral sprouting is a process whereby non-injured primary afferent neurons respond to some stimulus and extend new branches from existing axons. Neurons of both the central and peripheral nervous systems undergo this process, which contributes to both adaptive and maladaptive plasticity (e.g., [1], [2], [3], [4], [5], [6], [7], [8], [9]). In the model used here (the "spared dermatome" model), the intact sensory neurons respond to the denervation of adjacent areas of skin by ...[more]

PMID: 26697387

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Project description:Primary afferent collateral sprouting (PACS) is a process whereby non-injured primary afferent neurons respond to some stimulus by extending new branches from existing axons. In the model used here (spared dermatome), the intact sensory neurons respond to the denervation of adjacent areas of skin by sprouting new axon branches into that adjacent denervated territory. Neurons of both the central and peripheral nervous systems undergo this process, which contributes to both adaptive and maladaptive plasticity. Investigations of gene expression changes associated with PACS can provide a better understanding of the molecular mechanisms controlling this process. Consequently, it can be used to develop treatment for spinal cord injury to promote functional recovery. In this study, we sought to identify gene expression changes in PACS using 20 Affymetrix Rat Genome 230 2.0 microarrays. The experiments were designed to discover global gene expression changes in non-injured DRG neurons undergoing PACS. T11 DRG neurons remained intact and undergo PACS after the cutaneous nerves of the adjacent segments (T9, T10, T12, and T13) were injured and regeneration of those injured nerves prevented by ligation. Thus, the T9, T10, T12, and T13 dermatomes were denervated, but the T11 dermatome remained intact. Axons of the T11dermatome (and thus housed in the T11 dorsal root ganglion (DRG)), extended new branches to innervate the T9, T10, T12, and T13 dermatomes. N.B.: This is NOT a spared root experiment. ALL spinal roots were non-injured. Peripheral nerves were used. A total of 20 Affymetrix Rat Genome 230 2.0 microarrays were analyzed: six naÃ¯ve controls, seven replicates at day 7 post-surgery (presumed to represent an â??initiation phaseâ??), and seven replicates at day 14 post-surgery (presumed to represent a â??maintenance phaseâ??). DRGs were NOT pooled onto microarrays. Each animal had its own microarray with T11 DRG sample which underwent 2-round amplification. After quality control analysis, one of the naÃ¯ve control microarrays was removed from further analysis.

Project description:RationaleCoronary collateral growth is a natural bypass for ischemic heart diseases. It offers tremendous therapeutic benefit, but the process of coronary collateral growth isincompletely understood due to limited preclinical murine models that would enable interrogation of its mechanisms and processes via genetic modification and lineage tracing. Understanding the processes by which coronary collaterals develop can unlock new therapeutic strategies for ischemic heart disease.ObjectiveTo develop a murine model of coronary collateral growth by repetitive ischemia and investigate whether capillary endothelial cells could contribute to the coronary collateral formation in an adult mouse heart after repetitive ischemia by lineage tracing.Methods and resultsA murine model of coronary collateral growth was developed using short episodes of repetitive ischemia. Repetitive ischemia stimulation resulted in robust collateral growth in adult mouse hearts, validated by high-resolution micro-computed tomography. Repetitive ischemia-induced collateral formation compensated ischemia caused by occlusion of the left anterior descending artery. Cardiac function improved during ischemia after repetitive ischemia, suggesting the improvement of coronary blood flow. A capillary-specific Cre driver (Apln-CreER) was used for lineage tracing capillary endothelial cells. ROSA mT/mG reporter mice crossed with the Apln-CreER transgene mice underwent a 17 days' repetitive ischemia protocol for coronary collateral growth. Two-photon and confocal microscopy imaging of heart slices revealed repetitive ischemia-induced coronary collateral growth initiated from sprouting Apelin+ endothelial cells. Newly formed capillaries in the collateral-dependent zone expanded in diameter upon repetitive ischemia stimulation and arterialized with smooth muscle cell recruitment, forming mature coronary arteries. Notably, pre-existing coronary arteries and arterioles were not Apelin+, and all Apelin+ collaterals arose from sprouting capillaries. Cxcr4, Vegfr2, Jag1, Mcp1, and Hif1⍺ mRNA levels in the repetitive ischemia-induced hearts were also upregulated at the early stage of coronary collateral growth, suggesting angiogenic signaling pathways are activated for coronary collaterals formation during repetitive ischemia.ConclusionsWe developed a murine model of coronary collateral growth induced by repetitive ischemia. Our lineage tracing study shows that sprouting endothelial cells contribute to coronary collateral growth in adult mouse hearts. For the first time, sprouting angiogenesis is shown to give rise to mature coronary arteries in response to repetitive ischemia in the adult mouse hearts.

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Transcriptional changes in sensory ganglia associated with primary afferent axon collateral sprouting in spared dermatome model.

Publications

Transcriptional changes in sensory ganglia associated with primary afferent axon collateral sprouting in spared dermatome model.

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