Hepatic Sinusoidal Endothelial Cell Antibody [L23C8]

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution
WB1:400-1:2000 IHC1:400-1:2000

Application
WB, IHC, IF, FCM

Reactivity
Human, Mouse, Rat

Source
Mouse Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Datasheet & SDS

Biological Description

Specificity
Hepatic Sinusoidal Endothelial Cell Antibody [L23C8] detects levels of total Hepatic Sinusoidal Endothelial Cell.

Clone
L23C8

Synonym(s)
Hepatic cells, Hepatic Sinusoidal Endothelial Cells, HSE, SE1, Sinusoidal Endothelial Cells

Background
Hepatic sinusoidal endothelial cells (also termed liver sinusoidal endothelial cells, LSECs) form the highly specialized, fenestrated endothelial lining of hepatic sinusoids and constitute the interface between circulating blood components and parenchymal hepatocytes and hepatic stellate cells, where they coordinate filtration, scavenging, hemodynamic regulation, and immune surveillance in the liver microenvironment. The cells display a discontinuous endothelium with abundant transcellular fenestrations organized into sieve plates, lack an organized basement membrane, and exhibit close apposition of luminal and abluminal plasma membranes at sites beyond classical junctions, a structural configuration that permits efficient plasma ultrafiltration into the space of Disse while restricting passage of larger particles such as chylomicrons. This architecture creates low-resistance exchange for solutes, lipoproteins, and signaling molecules and positions LSECs to regulate hepatic microcirculation through production of nitric oxide and other vasoactive mediators that adjust sinusoidal tone and portal pressure in response to shear stress, metabolic cues, and neurohumoral signals. LSECs express high levels of scavenger, mannose, and Fcγ receptors and have exceptional endocytic capacity, enabling clearance of modified lipoproteins, glycosylated and immune complexes, hormones, and microbial products from the circulation and contributing to systemic homeostasis of lipids, metabolites, and pathogen-associated ligands. The cells also function as immunologically active sentinels that present antigen to T cells, induce tolerance in CD8⁺ T cells and regulatory T cell differentiation, and orchestrate leukocyte recruitment via regulated expression of adhesion molecules such as ICAM‑1, VCAM‑1, and VAP‑1, thereby shaping hepatic immune responses to gut-derived antigens, infections, and sterile injury. Crosstalk between LSECs and hepatic stellate cells through VEGF, CXCR7–Id1-driven angiocrine factors, and other paracrine mediators maintains stellate cell quiescence and supports liver regeneration after acute injury, while phenotypic changes in LSECs during chronic injury, including capillarization (loss of fenestrations and development of basement membrane), altered angiocrine signaling, and pro-fibrotic FGFR1 activation, promote fibrosis, portal hypertension, and progression to cirrhosis and hepatocellular carcinoma. Ageing and metabolic dysfunction-associated steatotic liver disease are associated with defenestration, reduced scavenger function, and impaired nitric oxide production in LSECs, changes that contribute to dysregulated lipid handling, sinusoidal resistance, and heightened susceptibility to inflammatory and neoplastic processes.

Background

Hepatic sinusoidal endothelial cells (also termed liver sinusoidal endothelial cells, LSECs) form the highly specialized, fenestrated endothelial lining of hepatic sinusoids and constitute the interface between circulating blood components and parenchymal hepatocytes and hepatic stellate cells, where they coordinate filtration, scavenging, hemodynamic regulation, and immune surveillance in the liver microenvironment. The cells display a discontinuous endothelium with abundant transcellular fenestrations organized into sieve plates, lack an organized basement membrane, and exhibit close apposition of luminal and abluminal plasma membranes at sites beyond classical junctions, a structural configuration that permits efficient plasma ultrafiltration into the space of Disse while restricting passage of larger particles such as chylomicrons. This architecture creates low-resistance exchange for solutes, lipoproteins, and signaling molecules and positions LSECs to regulate hepatic microcirculation through production of nitric oxide and other vasoactive mediators that adjust sinusoidal tone and portal pressure in response to shear stress, metabolic cues, and neurohumoral signals. LSECs express high levels of scavenger, mannose, and Fcγ receptors and have exceptional endocytic capacity, enabling clearance of modified lipoproteins, glycosylated and immune complexes, hormones, and microbial products from the circulation and contributing to systemic homeostasis of lipids, metabolites, and pathogen-associated ligands. The cells also function as immunologically active sentinels that present antigen to T cells, induce tolerance in CD8⁺ T cells and regulatory T cell differentiation, and orchestrate leukocyte recruitment via regulated expression of adhesion molecules such as ICAM‑1, VCAM‑1, and VAP‑1, thereby shaping hepatic immune responses to gut-derived antigens, infections, and sterile injury. Crosstalk between LSECs and hepatic stellate cells through VEGF, CXCR7–Id1-driven angiocrine factors, and other paracrine mediators maintains stellate cell quiescence and supports liver regeneration after acute injury, while phenotypic changes in LSECs during chronic injury, including capillarization (loss of fenestrations and development of basement membrane), altered angiocrine signaling, and pro-fibrotic FGFR1 activation, promote fibrosis, portal hypertension, and progression to cirrhosis and hepatocellular carcinoma. Ageing and metabolic dysfunction-associated steatotic liver disease are associated with defenestration, reduced scavenger function, and impaired nitric oxide production in LSECs, changes that contribute to dysregulated lipid handling, sinusoidal resistance, and heightened susceptibility to inflammatory and neoplastic processes.

References
https://pubmed.ncbi.nlm.nih.gov/12437787/ https://pubmed.ncbi.nlm.nih.gov/38943171/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%