scholarly journals Reduction of skin innervation is associated with a severe fibromyalgia phenotype

2019 ◽  
Vol 86 (4) ◽  
pp. 504-516 ◽  
Author(s):  
Dimitar Evdokimov ◽  
Johanna Frank ◽  
Alexander Klitsch ◽  
Stefan Unterecker ◽  
Bodo Warrings ◽  
...  
Keyword(s):  
Pain ◽  
2018 ◽  
pp. 1 ◽  
Author(s):  
Nurcan Üçeyler ◽  
Jan Vollert ◽  
Barbara Broll ◽  
Nadja Riediger ◽  
Melissa Langjahr ◽  
...  

2002 ◽  
Vol 448 (1) ◽  
pp. 28-52 ◽  
Author(s):  
Eva M.J. Peters ◽  
Vladimir A. Botchkarev ◽  
Sven Müller-Röver ◽  
Ingrid Moll ◽  
Frank L. Rice ◽  
...  

1999 ◽  
Vol 113 (6) ◽  
pp. 878-887 ◽  
Author(s):  
Vladimir A. Botchkarev ◽  
Eva M.J. Peters ◽  
Natalia V. Botchkareva ◽  
Marcus Maurer ◽  
Ralf Paus

2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
Roberta Lattanzi ◽  
Daniela Maftei ◽  
Veronica Marconi ◽  
Fulvio Florenzano ◽  
Silvia Franchi ◽  
...  

The new chemokine Prokineticin 2 (PROK2) and its receptors (PKR1and PKR2) have a role in inflammatory pain and immunomodulation. Here we identified PROK2 as a critical mediator of neuropathic pain in the chronic constriction injury (CCI) of the sciatic nerve in mice and demonstrated that blocking the prokineticin receptors with two PKR1-preferring antagonists (PC1 and PC7) reduces pain and nerve damage. PROK2 mRNA expression was upregulated in the injured nerve since day 3 post injury (dpi) and in the ipsilateral DRG since 6 dpi. PROK2 protein overexpression was evident in Schwann Cells, infiltrating macrophages and axons in the peripheral nerve and in the neuronal bodies and some satellite cells in the DRG. Therapeutic treatment of neuropathic mice with the PKR-antagonist, PC1, impaired the PROK2 upregulation and signalling. This fact, besides alleviating pain, brought down the burden of proinflammatory cytokines in the damaged nerve and prompted an anti-inflammatory repair program. Such a treatment also reduced intraneural oedema and axon degeneration as demonstrated by the physiological skin innervation and thickness conserved in CCI-PC1 mice. These findings suggest that PROK2 plays a crucial role in neuropathic pain and might represent a novel target of treatment for this disease.


1994 ◽  
Vol 131 (5) ◽  
pp. 742-743 ◽  
Author(s):  
L. Wang ◽  
M. Hilliges ◽  
M. Gajecki ◽  
J. A. Marcusson ◽  
O. Johansson

2021 ◽  
Vol Volume 14 ◽  
pp. 1573-1585
Author(s):  
Enriqueta Munoz-Islas ◽  
Cecilia Esther Elizondo-Martinez ◽  
Mariela Gutierrez-Lopez ◽  
Rosa Issel Acosta-Gonzalez ◽  
Veronica Zaga-Clavellina ◽  
...  

Biomolecules ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 1552
Author(s):  
Efrat Shavit-Stein ◽  
Shany Guly Gofrit ◽  
Alexandra Gayster ◽  
Yotam Teldan ◽  
Ariel Ron ◽  
...  

Diabetic peripheral neuropathy (DPN) is a disabling common complication of diabetes mellitus (DM). Thrombin, a coagulation factor, is increased in DM and affects nerve function via its G-protein coupled protease activated receptor 1 (PAR1). Methods: A novel PAR1 modulator (PARIN5) was designed based on the thrombin PAR1 recognition site. Coagulation, motor and sensory function and small fiber loss were evaluated by employing the murine streptozotocin diabetes model. Results: PARIN5 showed a safe coagulation profile and showed no significant effect on weight or glucose levels. Diabetic mice spent shorter time on the rotarod (p < 0.001), and had hypoalgesia (p < 0.05), slow conduction velocity (p < 0.0001) and reduced skin innervation (p < 0.0001). Treatment with PARIN5 significantly improved rotarod performance (p < 0.05), normalized hypoalgesia (p < 0.05), attenuated slowing of nerve conduction velocity (p < 0.05) and improved skin innervation (p <0.0001). Conclusion: PARIN5 is a novel pharmacological approach for prevention of DPN development, via PAR1 pathway modulation.


Sign in / Sign up

Export Citation Format

Share Document