TAM receptors mediate the Fpr2-driven pain resolution and fibrinolysis after nerve injury
Nerve injury causes neuropathic pain and multilevel nerve barrier disruption. Nerve barriers consist of perineurial, endothelial and myelin barriers. So far, it is unclear whether resealing nerve barriers fosters pain resolution and recovery. To this end, we analysed the nerve barrier property portf...
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creator | Hartmannsberger, Beate Ben-Kraiem, Adel Kramer, Sofia Guidolin, Carolina Kazerani, Ida Doppler, Kathrin Thomas, Dominique Gurke, Robert Sisignano, Marco Kalelkar, Pranav P. García, Andrés J. Monje, Paula V. Sammeth, Michael Nusrat, Asma Brack, Alexander Krug, Susanne M. Sommer, Claudia Rittner, Heike L. |
description | Nerve injury causes neuropathic pain and multilevel nerve barrier disruption. Nerve barriers consist of perineurial, endothelial and myelin barriers. So far, it is unclear whether resealing nerve barriers fosters pain resolution and recovery. To this end, we analysed the nerve barrier property portfolio, pain behaviour battery and lipidomics for precursors of specialized pro-resolving meditators (SPMs) and their receptors in chronic constriction injury of the rat sciatic nerve to identify targets for pain resolution by resealing the selected nerve barriers. Of the three nerve barriers—perineurium, capillaries and myelin—only capillary tightness specifically against larger molecules, such as fibrinogen, recuperated with pain resolution. Fibrinogen immunoreactivity was elevated in rats not only at the time of neuropathic pain but also in nerve biopsies from patients with (but not without) painful polyneuropathy, indicating that sealing of the vascular barrier might be a novel approach in pain treatment. Hydroxyeicosatetraenoic acid (15R-HETE), a precursor of aspirin-triggered lipoxin A4, was specifically upregulated at the beginning of pain resolution. Repeated local application of resolvin D1-laden nanoparticles or Fpr2 agonists sex-independently resulted in accelerated pain resolution and fibrinogen removal. Clearing macrophages (
Cd206)
were boosted and fibrinolytic pathways (
Plat)
were induced, while inflammation (
Tnfα)
and inflammasomes (
Nlrp3)
were unaffected by this treatment. Blocking TAM receptors (Tyro3, Axl and Mer) and tyrosine kinase receptors linking haemostasis and inflammation completely inhibited all the effects. In summary, nanoparticles can be used as transporters for fleeting lipids, such as SPMs, and therefore expand the array of possible therapeutic agents. Thus, the Fpr2–Cd206–TAM receptor axis may be a suitable target for strengthening the capillary barrier, removing endoneurial fibrinogen and boosting pain resolution in patients with chronic neuropathic pain. |
doi_str_mv | 10.1007/s00401-024-02840-9 |
format | Article |
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Cd206)
were boosted and fibrinolytic pathways (
Plat)
were induced, while inflammation (
Tnfα)
and inflammasomes (
Nlrp3)
were unaffected by this treatment. Blocking TAM receptors (Tyro3, Axl and Mer) and tyrosine kinase receptors linking haemostasis and inflammation completely inhibited all the effects. In summary, nanoparticles can be used as transporters for fleeting lipids, such as SPMs, and therefore expand the array of possible therapeutic agents. Thus, the Fpr2–Cd206–TAM receptor axis may be a suitable target for strengthening the capillary barrier, removing endoneurial fibrinogen and boosting pain resolution in patients with chronic neuropathic pain.</description><identifier>ISSN: 0001-6322</identifier><identifier>ISSN: 1432-0533</identifier><identifier>EISSN: 1432-0533</identifier><identifier>DOI: 10.1007/s00401-024-02840-9</identifier><identifier>PMID: 39680199</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Aspirin ; Axl protein ; Biopsy ; Capillaries ; Chronic pain ; Docosahexaenoic Acids - pharmacology ; Female ; Fibrin ; Fibrinogen ; Fibrinolysis ; Humans ; Immunoreactivity ; Inflammasomes ; Inflammation ; Lipids ; Lipoxin A4 ; Macrophages ; Male ; Medicine ; Medicine & Public Health ; Myelin ; Nanoparticles ; Neuralgia ; Neuralgia - metabolism ; Neuralgia - pathology ; Neurosciences ; Original Paper ; Pain ; Pathology ; Perineurium ; Peripheral Nerve Injuries - metabolism ; Polyneuropathy ; Protein-tyrosine kinase receptors ; Rats ; Rats, Sprague-Dawley ; Receptor mechanisms ; Receptors, Formyl Peptide - metabolism ; Receptors, Lipoxin - metabolism ; Sciatic nerve ; Sciatic Nerve - injuries</subject><ispartof>Acta neuropathologica, 2024-12, Vol.149 (1), p.1</ispartof><rights>The Author(s) 2024</rights><rights>2024. The Author(s).</rights><rights>Copyright Springer Nature B.V. Jun 2025</rights><rights>The Author(s) 2024 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00401-024-02840-9$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00401-024-02840-9$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39680199$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hartmannsberger, Beate</creatorcontrib><creatorcontrib>Ben-Kraiem, Adel</creatorcontrib><creatorcontrib>Kramer, Sofia</creatorcontrib><creatorcontrib>Guidolin, Carolina</creatorcontrib><creatorcontrib>Kazerani, Ida</creatorcontrib><creatorcontrib>Doppler, Kathrin</creatorcontrib><creatorcontrib>Thomas, Dominique</creatorcontrib><creatorcontrib>Gurke, Robert</creatorcontrib><creatorcontrib>Sisignano, Marco</creatorcontrib><creatorcontrib>Kalelkar, Pranav P.</creatorcontrib><creatorcontrib>García, Andrés J.</creatorcontrib><creatorcontrib>Monje, Paula V.</creatorcontrib><creatorcontrib>Sammeth, Michael</creatorcontrib><creatorcontrib>Nusrat, Asma</creatorcontrib><creatorcontrib>Brack, Alexander</creatorcontrib><creatorcontrib>Krug, Susanne M.</creatorcontrib><creatorcontrib>Sommer, Claudia</creatorcontrib><creatorcontrib>Rittner, Heike L.</creatorcontrib><title>TAM receptors mediate the Fpr2-driven pain resolution and fibrinolysis after nerve injury</title><title>Acta neuropathologica</title><addtitle>Acta Neuropathol</addtitle><addtitle>Acta Neuropathol</addtitle><description>Nerve injury causes neuropathic pain and multilevel nerve barrier disruption. Nerve barriers consist of perineurial, endothelial and myelin barriers. So far, it is unclear whether resealing nerve barriers fosters pain resolution and recovery. To this end, we analysed the nerve barrier property portfolio, pain behaviour battery and lipidomics for precursors of specialized pro-resolving meditators (SPMs) and their receptors in chronic constriction injury of the rat sciatic nerve to identify targets for pain resolution by resealing the selected nerve barriers. Of the three nerve barriers—perineurium, capillaries and myelin—only capillary tightness specifically against larger molecules, such as fibrinogen, recuperated with pain resolution. Fibrinogen immunoreactivity was elevated in rats not only at the time of neuropathic pain but also in nerve biopsies from patients with (but not without) painful polyneuropathy, indicating that sealing of the vascular barrier might be a novel approach in pain treatment. Hydroxyeicosatetraenoic acid (15R-HETE), a precursor of aspirin-triggered lipoxin A4, was specifically upregulated at the beginning of pain resolution. Repeated local application of resolvin D1-laden nanoparticles or Fpr2 agonists sex-independently resulted in accelerated pain resolution and fibrinogen removal. Clearing macrophages (
Cd206)
were boosted and fibrinolytic pathways (
Plat)
were induced, while inflammation (
Tnfα)
and inflammasomes (
Nlrp3)
were unaffected by this treatment. Blocking TAM receptors (Tyro3, Axl and Mer) and tyrosine kinase receptors linking haemostasis and inflammation completely inhibited all the effects. In summary, nanoparticles can be used as transporters for fleeting lipids, such as SPMs, and therefore expand the array of possible therapeutic agents. Thus, the Fpr2–Cd206–TAM receptor axis may be a suitable target for strengthening the capillary barrier, removing endoneurial fibrinogen and boosting pain resolution in patients with chronic neuropathic pain.</description><subject>Animals</subject><subject>Aspirin</subject><subject>Axl protein</subject><subject>Biopsy</subject><subject>Capillaries</subject><subject>Chronic pain</subject><subject>Docosahexaenoic Acids - pharmacology</subject><subject>Female</subject><subject>Fibrin</subject><subject>Fibrinogen</subject><subject>Fibrinolysis</subject><subject>Humans</subject><subject>Immunoreactivity</subject><subject>Inflammasomes</subject><subject>Inflammation</subject><subject>Lipids</subject><subject>Lipoxin A4</subject><subject>Macrophages</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Myelin</subject><subject>Nanoparticles</subject><subject>Neuralgia</subject><subject>Neuralgia - metabolism</subject><subject>Neuralgia - pathology</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Pain</subject><subject>Pathology</subject><subject>Perineurium</subject><subject>Peripheral Nerve Injuries - metabolism</subject><subject>Polyneuropathy</subject><subject>Protein-tyrosine kinase receptors</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor mechanisms</subject><subject>Receptors, Formyl Peptide - metabolism</subject><subject>Receptors, Lipoxin - metabolism</subject><subject>Sciatic nerve</subject><subject>Sciatic Nerve - injuries</subject><issn>0001-6322</issn><issn>1432-0533</issn><issn>1432-0533</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><recordid>eNpdkc1O3DAUha0KVKa0L9AFssSmmxRf_8TJqkIIChKIDSxYWY5jDx5l7NRORpq3r-lMW2BxZV2dT0fn-iD0Fch3IESeZUI4gYpQXqbhpGo_oAVwRisiGDtAC0KKXDNKj9CnnFdlo5KLj-iItXVDoG0X6Onh_A4na-w4xZTx2vZeTxZPzxZfjYlWffIbG_CofShYjsM8-RiwDj12vks-xGGbfcbaTTbhYNPGYh9Wc9p-RodOD9l-2b_H6PHq8uHiurq9_3lzcX5bjdDwtuLCMUHrnhEnBal7w50zrawNla6RjDddA1LXFDQTstwGTBshXaeBdpwaw47Rj53vOHclvrFhSnpQY_JrnbYqaq_eKsE_q2XcKICatxKa4vBt75Dir9nmSa19NnYYdLBxzooBrxvBKKcFPX2HruKcQrnvhRKlBZBQqJPXkf5l-fvtBWA7IBcpLG36bwNEvZSrduWqUq76U65q2W_qUJTF</recordid><startdate>20241216</startdate><enddate>20241216</enddate><creator>Hartmannsberger, Beate</creator><creator>Ben-Kraiem, Adel</creator><creator>Kramer, Sofia</creator><creator>Guidolin, Carolina</creator><creator>Kazerani, Ida</creator><creator>Doppler, Kathrin</creator><creator>Thomas, Dominique</creator><creator>Gurke, Robert</creator><creator>Sisignano, Marco</creator><creator>Kalelkar, Pranav P.</creator><creator>García, Andrés J.</creator><creator>Monje, Paula V.</creator><creator>Sammeth, Michael</creator><creator>Nusrat, Asma</creator><creator>Brack, Alexander</creator><creator>Krug, Susanne M.</creator><creator>Sommer, Claudia</creator><creator>Rittner, Heike L.</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20241216</creationdate><title>TAM receptors mediate the Fpr2-driven pain resolution and fibrinolysis after nerve injury</title><author>Hartmannsberger, Beate ; Ben-Kraiem, Adel ; Kramer, Sofia ; Guidolin, Carolina ; Kazerani, Ida ; Doppler, Kathrin ; Thomas, Dominique ; Gurke, Robert ; Sisignano, Marco ; Kalelkar, Pranav P. ; García, Andrés J. ; Monje, Paula V. ; Sammeth, Michael ; Nusrat, Asma ; Brack, Alexander ; Krug, Susanne M. ; Sommer, Claudia ; Rittner, Heike L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p1849-45f3526d30f7506dc4ffc976c27f87348b817a621a35743213ac57fba12b42cc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Aspirin</topic><topic>Axl protein</topic><topic>Biopsy</topic><topic>Capillaries</topic><topic>Chronic pain</topic><topic>Docosahexaenoic Acids - pharmacology</topic><topic>Female</topic><topic>Fibrin</topic><topic>Fibrinogen</topic><topic>Fibrinolysis</topic><topic>Humans</topic><topic>Immunoreactivity</topic><topic>Inflammasomes</topic><topic>Inflammation</topic><topic>Lipids</topic><topic>Lipoxin A4</topic><topic>Macrophages</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Myelin</topic><topic>Nanoparticles</topic><topic>Neuralgia</topic><topic>Neuralgia - metabolism</topic><topic>Neuralgia - pathology</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>Pain</topic><topic>Pathology</topic><topic>Perineurium</topic><topic>Peripheral Nerve Injuries - metabolism</topic><topic>Polyneuropathy</topic><topic>Protein-tyrosine kinase receptors</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor mechanisms</topic><topic>Receptors, Formyl Peptide - metabolism</topic><topic>Receptors, Lipoxin - metabolism</topic><topic>Sciatic nerve</topic><topic>Sciatic Nerve - injuries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hartmannsberger, Beate</creatorcontrib><creatorcontrib>Ben-Kraiem, Adel</creatorcontrib><creatorcontrib>Kramer, Sofia</creatorcontrib><creatorcontrib>Guidolin, Carolina</creatorcontrib><creatorcontrib>Kazerani, Ida</creatorcontrib><creatorcontrib>Doppler, Kathrin</creatorcontrib><creatorcontrib>Thomas, Dominique</creatorcontrib><creatorcontrib>Gurke, Robert</creatorcontrib><creatorcontrib>Sisignano, Marco</creatorcontrib><creatorcontrib>Kalelkar, Pranav P.</creatorcontrib><creatorcontrib>García, Andrés J.</creatorcontrib><creatorcontrib>Monje, Paula V.</creatorcontrib><creatorcontrib>Sammeth, Michael</creatorcontrib><creatorcontrib>Nusrat, Asma</creatorcontrib><creatorcontrib>Brack, Alexander</creatorcontrib><creatorcontrib>Krug, Susanne M.</creatorcontrib><creatorcontrib>Sommer, Claudia</creatorcontrib><creatorcontrib>Rittner, Heike L.</creatorcontrib><collection>Springer Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Acta neuropathologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hartmannsberger, Beate</au><au>Ben-Kraiem, Adel</au><au>Kramer, Sofia</au><au>Guidolin, Carolina</au><au>Kazerani, Ida</au><au>Doppler, Kathrin</au><au>Thomas, Dominique</au><au>Gurke, Robert</au><au>Sisignano, Marco</au><au>Kalelkar, Pranav P.</au><au>García, Andrés J.</au><au>Monje, Paula V.</au><au>Sammeth, Michael</au><au>Nusrat, Asma</au><au>Brack, Alexander</au><au>Krug, Susanne M.</au><au>Sommer, Claudia</au><au>Rittner, Heike L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TAM receptors mediate the Fpr2-driven pain resolution and fibrinolysis after nerve injury</atitle><jtitle>Acta neuropathologica</jtitle><stitle>Acta Neuropathol</stitle><addtitle>Acta Neuropathol</addtitle><date>2024-12-16</date><risdate>2024</risdate><volume>149</volume><issue>1</issue><spage>1</spage><pages>1-</pages><issn>0001-6322</issn><issn>1432-0533</issn><eissn>1432-0533</eissn><abstract>Nerve injury causes neuropathic pain and multilevel nerve barrier disruption. Nerve barriers consist of perineurial, endothelial and myelin barriers. So far, it is unclear whether resealing nerve barriers fosters pain resolution and recovery. To this end, we analysed the nerve barrier property portfolio, pain behaviour battery and lipidomics for precursors of specialized pro-resolving meditators (SPMs) and their receptors in chronic constriction injury of the rat sciatic nerve to identify targets for pain resolution by resealing the selected nerve barriers. Of the three nerve barriers—perineurium, capillaries and myelin—only capillary tightness specifically against larger molecules, such as fibrinogen, recuperated with pain resolution. Fibrinogen immunoreactivity was elevated in rats not only at the time of neuropathic pain but also in nerve biopsies from patients with (but not without) painful polyneuropathy, indicating that sealing of the vascular barrier might be a novel approach in pain treatment. Hydroxyeicosatetraenoic acid (15R-HETE), a precursor of aspirin-triggered lipoxin A4, was specifically upregulated at the beginning of pain resolution. Repeated local application of resolvin D1-laden nanoparticles or Fpr2 agonists sex-independently resulted in accelerated pain resolution and fibrinogen removal. Clearing macrophages (
Cd206)
were boosted and fibrinolytic pathways (
Plat)
were induced, while inflammation (
Tnfα)
and inflammasomes (
Nlrp3)
were unaffected by this treatment. Blocking TAM receptors (Tyro3, Axl and Mer) and tyrosine kinase receptors linking haemostasis and inflammation completely inhibited all the effects. In summary, nanoparticles can be used as transporters for fleeting lipids, such as SPMs, and therefore expand the array of possible therapeutic agents. Thus, the Fpr2–Cd206–TAM receptor axis may be a suitable target for strengthening the capillary barrier, removing endoneurial fibrinogen and boosting pain resolution in patients with chronic neuropathic pain.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>39680199</pmid><doi>10.1007/s00401-024-02840-9</doi><oa>free_for_read</oa></addata></record> |
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subjects | Animals Aspirin Axl protein Biopsy Capillaries Chronic pain Docosahexaenoic Acids - pharmacology Female Fibrin Fibrinogen Fibrinolysis Humans Immunoreactivity Inflammasomes Inflammation Lipids Lipoxin A4 Macrophages Male Medicine Medicine & Public Health Myelin Nanoparticles Neuralgia Neuralgia - metabolism Neuralgia - pathology Neurosciences Original Paper Pain Pathology Perineurium Peripheral Nerve Injuries - metabolism Polyneuropathy Protein-tyrosine kinase receptors Rats Rats, Sprague-Dawley Receptor mechanisms Receptors, Formyl Peptide - metabolism Receptors, Lipoxin - metabolism Sciatic nerve Sciatic Nerve - injuries |
title | TAM receptors mediate the Fpr2-driven pain resolution and fibrinolysis after nerve injury |
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