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Peer-reviewedCC BY 4.0Bioscience Reports

Design of short-sequenced collagen type III-derived peptides with GPR56 dependent biological activity

  • Israa Mohammed Al-Amily1
  • Fariborz Parandeh1
  • Pontus Dunér2
  • Marie Sjögren1
  • Albert Salehi1
  1. 1Department of Clinical Science, Malmö, Division of Islet Cell Physiology, University of Lund, Sweden
  2. 2Department of Clinical Science, Malmö, Division of Experimental Cardiovascular Research, University of Lund, Sweden
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Abstract

We have previously shown that activation of G protein-coupled receptor 56 (GPR56) by its endogenous ligand collagen type III (Coll III) improves pancreatic β-cell function and potentiates glucose-stimulated insulin secretion (GSIS). In the present study, alignment of Coll III and GPR56 genomic DNA revealed three complementary nucleotide regions, enabling the design of three short peptides (NQGCKL·NH2, H·LLSSR·NH2, and NH2·GYYCG·COOH). The peptides in double or triple combinations markedly increased cellular cAMP levels, enhanced GSIS, and improved cell viability both in human (EndoC βH1 cells) and rat pancreatic β-cell lines (INS-1 832/13 cells). These effects were markedly absent in GPR56-knockdown cells, supporting receptor-dependent specificity. The peptide mixtures also counteracted cytokine- and glucotoxicity-induced cellular stress, restoring cAMP generation and insulin secretion. Comparable effects were not observed with dapagliflozin, while glibenclamide decreased cell viability under similar conditions. In hepatic cell lines (HepG2 and Hep1–6), peptide combinations enhanced cell survival in a GPR56-dependent manner, consistent with a broader role of GPR56 in metabolic regulation. Collectively, the data identify three short sequence collagen III-derived peptides whose biological effects are dependent on GPR56 expression and support their further investigation as tools for studying GPR56-associated cellular signaling for the future in vivo validation.

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Cite

BibTeXRIS
BibTeX
@article{alamily2026design,
  title = {{Design of short-sequenced collagen type III-derived peptides with GPR56 dependent biological activity}},
  author = {Israa Mohammed Al-Amily and Fariborz Parandeh and Pontus Dunér and Marie Sjögren and Albert Salehi},
  journal = {Bioscience Reports},
  year = {2026},
  month = nov,
  doi = {10.1042/bsr20250320},
  url = {https://doi.org/10.1042/bsr20250320},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Design of short-sequenced collagen type III-derived peptides with GPR56 dependent biological activity
AU  - Israa Mohammed Al-Amily
AU  - Fariborz Parandeh
AU  - Pontus Dunér
AU  - Marie Sjögren
AU  - Albert Salehi
PY  - 2026
DA  - 2026/11/03
JO  - Bioscience Reports
DO  - 10.1042/bsr20250320
UR  - https://doi.org/10.1042/bsr20250320
AB  - We have previously shown that activation of G protein-coupled receptor 56 (GPR56) by its endogenous ligand collagen type III (Coll III) improves pancreatic β-cell function and potentiates glucose-stimulated insulin secretion (GSIS). In the present study, alignment of Coll III and GPR56 genomic DNA revealed three complementary nucleotide regions, enabling the design of three short peptides (NQGCKL·NH2, H·LLSSR·NH2, and NH2·GYYCG·COOH). The peptides in double or triple combinations markedly increased cellular cAMP levels, enhanced GSIS, and improved cell viability both in human (EndoC βH1 cells) and rat pancreatic β-cell lines (INS-1 832/13 cells). These effects were markedly absent in GPR56-knockdown cells, supporting receptor-dependent specificity. The peptide mixtures also counteracted cytokine- and glucotoxicity-induced cellular stress, restoring cAMP generation and insulin secretion. Comparable effects were not observed with dapagliflozin, while glibenclamide decreased cell viability under similar conditions. In hepatic cell lines (HepG2 and Hep1–6), peptide combinations enhanced cell survival in a GPR56-dependent manner, consistent with a broader role of GPR56 in metabolic regulation. Collectively, the data identify three short sequence collagen III-derived peptides whose biological effects are dependent on GPR56 expression and support their further investigation as tools for studying GPR56-associated cellular signaling for the future in vivo validation.
SN  - 0144-8463
SN  - 1573-4935
ER  -