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Moderation of skeletal muscle reperfusion injury by a sLe(x)-glycosylated complement inhibitory protein.
Am J Physiol Cell Physiol. 2001 Jul; 281(1):C224-30.AJ

Abstract

The role of the sialyl Lewis(x) (sLe(x))-decorated version of soluble complement receptor type 1 (sCR1) in moderating skeletal muscle reperfusion injury, by antagonizing neutrophil endothelial selectin interaction and complement activation, is examined. Mice underwent 2 h of hindlimb ischemia and 3 h of reperfusion. Permeability index (PI) was assessed by extravasation of 125I-labeled albumin. Neutrophil depletion and complement inhibition with sCR1 reduced permeability by 72% (PI 0.81 +/- 0.10) compared with a 42% decrease (PI 1.53 +/- 0.08) observed in neutropenic mice, indicating that part of the complement-mediated injury is neutrophil independent. sCR1sLe(x) treatment reduced PI by 70% (PI 0.86 +/- 0.06), an additional 20% decrease compared with sCR1 treatment (PI 1.32 +/- 0.08). Treatment with sCR1sLe(x) 0.5 and 1 h after reperfusion reduced permeability by 63% (PI 0.09 +/- 0.07) and 52% (PI 1.24 +/- 0.09), respectively, compared with the respective decreases of 41% (PI 1.41 +/- 0.10) and 32% (PI 1.61 +/- 0.07) after sCR1 treatment. Muscle immunohistochemistry stained for sCR1 only on the vascular endothelium of sCR1sLe(x)-treated mice. In conclusion, sCR1sLe(x) is more effective than sCR1 in moderating skeletal muscle reperfusion injury.

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Authors+Show Affiliations

Kyriakides C
Department of Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Wang Y
No affiliation info available
Austen WG
No affiliation info available
Favuzza J
No affiliation info available
Kobzik L
No affiliation info available
Moore FD
No affiliation info available
Hechtman HB
No affiliation info available

MeSH

AnimalsCell Membrane PermeabilityComplement ActivationComplement Inactivator ProteinsHindlimbImmunohistochemistryMaleMiceMice, Inbred C57BLMuscle, SkeletalNeutrophilsOligosaccharidesReceptors, ComplementRecombinant ProteinsReperfusion InjurySialyl Lewis X Antigen

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11401845

Citation

Kyriakides, C, et al. "Moderation of Skeletal Muscle Reperfusion Injury By a sLe(x)-glycosylated Complement Inhibitory Protein." American Journal of Physiology. Cell Physiology, vol. 281, no. 1, 2001, pp. C224-30.
Kyriakides C, Wang Y, Austen WG, et al. Moderation of skeletal muscle reperfusion injury by a sLe(x)-glycosylated complement inhibitory protein. Am J Physiol Cell Physiol. 2001;281(1):C224-30.
Kyriakides, C., Wang, Y., Austen, W. G., Favuzza, J., Kobzik, L., Moore, F. D., & Hechtman, H. B. (2001). Moderation of skeletal muscle reperfusion injury by a sLe(x)-glycosylated complement inhibitory protein. American Journal of Physiology. Cell Physiology, 281(1), C224-30.
Kyriakides C, et al. Moderation of Skeletal Muscle Reperfusion Injury By a sLe(x)-glycosylated Complement Inhibitory Protein. Am J Physiol Cell Physiol. 2001;281(1):C224-30. PubMed PMID: 11401845.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Moderation of skeletal muscle reperfusion injury by a sLe(x)-glycosylated complement inhibitory protein. AU - Kyriakides,C, AU - Wang,Y, AU - Austen,W G,Jr AU - Favuzza,J, AU - Kobzik,L, AU - Moore,F D,Jr AU - Hechtman,H B, PY - 2001/6/13/pubmed PY - 2001/7/13/medline PY - 2001/6/13/entrez SP - C224 EP - 30 JF - American journal of physiology. Cell physiology JO - Am J Physiol Cell Physiol VL - 281 IS - 1 N2 - The role of the sialyl Lewis(x) (sLe(x))-decorated version of soluble complement receptor type 1 (sCR1) in moderating skeletal muscle reperfusion injury, by antagonizing neutrophil endothelial selectin interaction and complement activation, is examined. Mice underwent 2 h of hindlimb ischemia and 3 h of reperfusion. Permeability index (PI) was assessed by extravasation of 125I-labeled albumin. Neutrophil depletion and complement inhibition with sCR1 reduced permeability by 72% (PI 0.81 +/- 0.10) compared with a 42% decrease (PI 1.53 +/- 0.08) observed in neutropenic mice, indicating that part of the complement-mediated injury is neutrophil independent. sCR1sLe(x) treatment reduced PI by 70% (PI 0.86 +/- 0.06), an additional 20% decrease compared with sCR1 treatment (PI 1.32 +/- 0.08). Treatment with sCR1sLe(x) 0.5 and 1 h after reperfusion reduced permeability by 63% (PI 0.09 +/- 0.07) and 52% (PI 1.24 +/- 0.09), respectively, compared with the respective decreases of 41% (PI 1.41 +/- 0.10) and 32% (PI 1.61 +/- 0.07) after sCR1 treatment. Muscle immunohistochemistry stained for sCR1 only on the vascular endothelium of sCR1sLe(x)-treated mice. In conclusion, sCR1sLe(x) is more effective than sCR1 in moderating skeletal muscle reperfusion injury. SN - 0363-6143 UR - https://www.unboundmedicine.com/medline/citation/11401845/Moderation_of_skeletal_muscle_reperfusion_injury_by_a_sLe_x__glycosylated_complement_inhibitory_protein_ L2 - https://journals.physiology.org/doi/10.1152/ajpcell.2001.281.1.C224?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -