Linking the Pathobiology of Hypercholesterolemia with the Neutrophil Mechanotransduction

Zhang, Xiaoyan; Shin, Hainsworth Y.

doi:10.5772/47867

Lipoproteins - Role in Health and Diseases 2012

DOI: 10.5772/47867

|View full text |Cite

Linking the Pathobiology of Hypercholesterolemia with the Neutrophil Mechanotransduction

Xiaoyan Zhang¹,

Hainsworth Y. Shin²

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2013

Publication Types

Select...

Article1

Relationship

Self Cite0

Independent1

Authors

Journals

Cited by 1 publication

References 136 publications

(202 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

Characterization of the shear stress regulation of CD18 surface expression by HL60-derived neutrophil-like cells

Akenhead

Zhang

Shin

2013

Biomech Model Mechanobiol

View full text Add to dashboard Cite

Shear stress-induced cleavage of cell surface CD18 integrins is reported to be part of an anti-inflammatory control mechanism that minimizes neutrophil activity in the blood under physiologic conditions. The cysteine protease, cathepsin B (catB), has been implicated in this mechanoregulatory mechanism, but its molecular dynamics remain to be elucidated. Moreover, attempts to do so using molecular approaches are hindered by the limited ex vivo life span of primary neutrophils. As an alternative, we explored the potential use of HL60-derived neutrophilic cells as a transfectable culture model that exhibits a shear-induced CD18 cleavage response comparable to primary neutrophils. HL60 cells were differentiated into neutrophil-like cells (dHL60-NCs) and exposed to laminar shear stress ([Formula: see text] for 10 min). Based on cytometric analyses, sheared cells cleaved CD18 and CD11a, but not CD11b, integrins. Treatment of cells with E64 or doxycycline prior to and during shear exposure inhibited CD18, but only attenuated CD11a, cleavage. Neither aprotinin nor pepstatin affected shear-induced CD18 or CD11a cleavage. Notably, dHL60-NCs expressed minimal catB. Thus, multiple cysteine proteases in addition to catB may cleave CD18 on sheared leukocytes. In fact, our findings indicate that multiple non-cysteine proteases also participate in the shear-related cleavage of CD11/CD18 heterodimers. Finally, shear-induced cleavage of CD18 and CD11a by dHL60-NCs was inhibited by fMLP concentrations of at least [Formula: see text]. Collectively, our findings indicate that shear-induced CD11/CD18 cleavage is phenotypic of neutrophilic cells, including those derived from HL60 cells. Moreover, our results verify shear stress as a key anti-inflammatory stimulus for neutrophils under physiologic conditions.

show abstract

Characterization of the shear stress regulation of CD18 surface expression by HL60-derived neutrophil-like cells

Akenhead

Zhang

Shin

2013

Biomech Model Mechanobiol

View full text Add to dashboard Cite

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

Linking the Pathobiology of Hypercholesterolemia with the Neutrophil Mechanotransduction

Cited by 1 publication

References 136 publications

Characterization of the shear stress regulation of CD18 surface expression by HL60-derived neutrophil-like cells

Characterization of the shear stress regulation of CD18 surface expression by HL60-derived neutrophil-like cells

Contact Info

Product

Resources

About