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Blockade of transient receptor potential cation channel subfamily V member 1 promotes regeneration after sciatic nerve injury.

Ren F, Zhang H, Qi C, Gao ML, Wang H, Li XQ - Neural Regen Res (2015)

Bottom Line: TRPV1 expression in the injured sciatic nerve and ipsilateral dorsal root ganglia was markedly greater than on the contralateral side.Pretreatment with AMG517 blocked this effect.These data indicate that TRPV1 is activated or overexpressed after sciatic nerve crush injury, and that blockade of TRPV1 may accelerate regeneration of the injured sciatic nerve.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathophysiology, School of Basic Medical Sciences, Shanxi Medical University, Taiyuan, Shanxi Province, China.

ABSTRACT
The transient receptor potential cation channel subfamily V member 1 (TRPV1) provides the sensation of pain (nociception). However, it remains unknown whether TRPV1 is activated after peripheral nerve injury, or whether activation of TRPV1 affects neural regeneration. In the present study, we established rat models of unilateral sciatic nerve crush injury, with or without pretreatment with AMG517 (300 mg/kg), a TRPV1 antagonist, injected subcutaneously into the ipsilateral paw 60 minutes before injury. At 1 and 2 weeks after injury, we performed immunofluorescence staining of the sciatic nerve at the center of injury, at 0.3 cm proximal and distal to the injury site, and in the dorsal root ganglia. Our results showed that Wallerian degeneration occurred distal to the injury site, and neurite outgrowth and Schwann cell regeneration occurred proximal to the injury. The number of regenerating myelinated and unmyelinated nerve clusters was greater in the AMG517-pretreated rats than in the vehicle-treated group, most notably 2 weeks after injury. TRPV1 expression in the injured sciatic nerve and ipsilateral dorsal root ganglia was markedly greater than on the contralateral side. Pretreatment with AMG517 blocked this effect. These data indicate that TRPV1 is activated or overexpressed after sciatic nerve crush injury, and that blockade of TRPV1 may accelerate regeneration of the injured sciatic nerve.

No MeSH data available.


Related in: MedlinePlus

TRPV1 immunofluorescence in longitudinal sections of sciatic nerve with or without crush injury.No TRPV1 immunofluorescence was observed in the uninjured sciatic nerve, except for a weak positive reaction in the nerve trunk. At 1 and 2 weeks after injury, TRPV1 immunoreactivity (green fluorescence) was notably greater than in the uninjured nerve, especially near the epineurium. In AMG517-pretreated animals, TRPV1 immunoreactivity was weaker 1 and 2 weeks after injury than in the untreated groups, but still stronger than that in the uninjured side. TRPV1: Transient receptor potential cation channel subfamily V member 1; AMG: AMG517 (TRPV1 antagonist). Scale bar: 50 μm.
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Figure 7: TRPV1 immunofluorescence in longitudinal sections of sciatic nerve with or without crush injury.No TRPV1 immunofluorescence was observed in the uninjured sciatic nerve, except for a weak positive reaction in the nerve trunk. At 1 and 2 weeks after injury, TRPV1 immunoreactivity (green fluorescence) was notably greater than in the uninjured nerve, especially near the epineurium. In AMG517-pretreated animals, TRPV1 immunoreactivity was weaker 1 and 2 weeks after injury than in the untreated groups, but still stronger than that in the uninjured side. TRPV1: Transient receptor potential cation channel subfamily V member 1; AMG: AMG517 (TRPV1 antagonist). Scale bar: 50 μm.

Mentions: Indirect immunofluorescence staining for TRPV1 was negative in longitudinal sections of normal sciatic nerve. However, positive TRPV1 staining was observed at the injury site 1 and 2 weeks after nerve crush. Positive fibers were scattered around the sciatic nerve, mainly near the epineurium. Compared with the vehicle-pretreated injury groups, TRPV1 expression was weaker in the groups that received AMG517, but was still stronger than that in the uninjured side (Figure 7).


Blockade of transient receptor potential cation channel subfamily V member 1 promotes regeneration after sciatic nerve injury.

Ren F, Zhang H, Qi C, Gao ML, Wang H, Li XQ - Neural Regen Res (2015)

TRPV1 immunofluorescence in longitudinal sections of sciatic nerve with or without crush injury.No TRPV1 immunofluorescence was observed in the uninjured sciatic nerve, except for a weak positive reaction in the nerve trunk. At 1 and 2 weeks after injury, TRPV1 immunoreactivity (green fluorescence) was notably greater than in the uninjured nerve, especially near the epineurium. In AMG517-pretreated animals, TRPV1 immunoreactivity was weaker 1 and 2 weeks after injury than in the untreated groups, but still stronger than that in the uninjured side. TRPV1: Transient receptor potential cation channel subfamily V member 1; AMG: AMG517 (TRPV1 antagonist). Scale bar: 50 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4590249&req=5

Figure 7: TRPV1 immunofluorescence in longitudinal sections of sciatic nerve with or without crush injury.No TRPV1 immunofluorescence was observed in the uninjured sciatic nerve, except for a weak positive reaction in the nerve trunk. At 1 and 2 weeks after injury, TRPV1 immunoreactivity (green fluorescence) was notably greater than in the uninjured nerve, especially near the epineurium. In AMG517-pretreated animals, TRPV1 immunoreactivity was weaker 1 and 2 weeks after injury than in the untreated groups, but still stronger than that in the uninjured side. TRPV1: Transient receptor potential cation channel subfamily V member 1; AMG: AMG517 (TRPV1 antagonist). Scale bar: 50 μm.
Mentions: Indirect immunofluorescence staining for TRPV1 was negative in longitudinal sections of normal sciatic nerve. However, positive TRPV1 staining was observed at the injury site 1 and 2 weeks after nerve crush. Positive fibers were scattered around the sciatic nerve, mainly near the epineurium. Compared with the vehicle-pretreated injury groups, TRPV1 expression was weaker in the groups that received AMG517, but was still stronger than that in the uninjured side (Figure 7).

Bottom Line: TRPV1 expression in the injured sciatic nerve and ipsilateral dorsal root ganglia was markedly greater than on the contralateral side.Pretreatment with AMG517 blocked this effect.These data indicate that TRPV1 is activated or overexpressed after sciatic nerve crush injury, and that blockade of TRPV1 may accelerate regeneration of the injured sciatic nerve.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathophysiology, School of Basic Medical Sciences, Shanxi Medical University, Taiyuan, Shanxi Province, China.

ABSTRACT
The transient receptor potential cation channel subfamily V member 1 (TRPV1) provides the sensation of pain (nociception). However, it remains unknown whether TRPV1 is activated after peripheral nerve injury, or whether activation of TRPV1 affects neural regeneration. In the present study, we established rat models of unilateral sciatic nerve crush injury, with or without pretreatment with AMG517 (300 mg/kg), a TRPV1 antagonist, injected subcutaneously into the ipsilateral paw 60 minutes before injury. At 1 and 2 weeks after injury, we performed immunofluorescence staining of the sciatic nerve at the center of injury, at 0.3 cm proximal and distal to the injury site, and in the dorsal root ganglia. Our results showed that Wallerian degeneration occurred distal to the injury site, and neurite outgrowth and Schwann cell regeneration occurred proximal to the injury. The number of regenerating myelinated and unmyelinated nerve clusters was greater in the AMG517-pretreated rats than in the vehicle-treated group, most notably 2 weeks after injury. TRPV1 expression in the injured sciatic nerve and ipsilateral dorsal root ganglia was markedly greater than on the contralateral side. Pretreatment with AMG517 blocked this effect. These data indicate that TRPV1 is activated or overexpressed after sciatic nerve crush injury, and that blockade of TRPV1 may accelerate regeneration of the injured sciatic nerve.

No MeSH data available.


Related in: MedlinePlus