Novel epinephrine and cyclic AMP-mediated activation of BCAM/Lu-dependent sickle (SS) RBC adhesion

Hines, Patrick C.; Zen, Qin; Burney, Sharran N.; Shea, Deborah A.; Ataga, Kenneth I.; Orringer, Eugene P.; Telen, Marilyn J.; Parise, Leslie V.

doi:10.1182/blood-2001-12-0289

Cited by 156 publications

(194 citation statements)

References 35 publications

(31 reference statements)

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“…Evidence for activation of PKA was detectable in about half of the homozygous sickle cell patients we studied. Hines et al demonstrated recently that SS RBC from about 50% of patients could be stimulated by epinephrine via a PKA-dependent signaling pathway to increase B-CAM/LU-mediated adhesion [24]. While LD SS RBC were more responsive than HD SS RBC, when compared with their corresponding baselines, stimulated HD SS RBC still adhered to laminin more than did stimulated LD SS RBC [24].…”

Section: Discussionmentioning

confidence: 99%

“…Previous work has shown that mature RBC have a number of signaling molecules and protein kinases, including protein kinase A and several tyrosine kinases [27]. A recent report also demonstrated that stimulation of a PKA-signaling pathway in vitro up-regulated B-CAM/LU-mediated adhesion to immobilized laminin during continuous flow [24]. We hypothesized that this pathway might be activated either in vivo or in response to shear stress in vitro.…”

Section: Evidence That Protein Kinase a Contributes To Increased Hd Smentioning

confidence: 91%

“…For inhibition assays using soluble recombinant Lutheran extracellular domain fragment (srLU) [24], 100 mg/ml of srLU or BSA was added onto the laminin-coated slide at room temperature for 1 hr. Chambers were washed with PBS before SS RBC were infused into the chamber.…”

Section: Flow Chamber Assaysmentioning

confidence: 99%

“…They also showed that membrane protein phosphorylation is altered when SS RBC are exposed to shear stress [23]. Another recent study showed that SS RBC adhesion to laminin was enhanced by activation of protein kinase A [24]. While the degree of activation of B-CAM/LU produced in vitro was more pronounced for LD SS RBC than HD SS RBC, activated HD SS RBC still adhered to laminin more strongly than did LD SS RBC during continuous flow at 1 dyne/cm 2 [24].…”

Section: Introductionmentioning

confidence: 96%

“…Another recent study showed that SS RBC adhesion to laminin was enhanced by activation of protein kinase A [24]. While the degree of activation of B-CAM/LU produced in vitro was more pronounced for LD SS RBC than HD SS RBC, activated HD SS RBC still adhered to laminin more strongly than did LD SS RBC during continuous flow at 1 dyne/cm 2 [24]. Third, mechanical factors-including the less spherical shape and higher density of HD SS RBC-may also play a role in cell adhesion to laminin under dynamic flow conditions.…”

Section: Introductionmentioning

confidence: 99%

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B‐CAM/LU expression and the role of B‐CAM/LU activation in binding of low‐ and high‐density red cells to laminin in sickle cell disease

et al. 2004

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Red blood cells from patients with sickle cell disease (SS RBC) adhere to laminin and over-express the high-affinity laminin receptor basal cell adhesion molecule/Lutheran protein (B-CAM/LU). This receptor has recently been shown to undergo activation in vitro through a protein kinase A-dependent mechanism. Low-density SS RBC express twothirds more B-CAM/LU than high-density SS RBC. However, high-density SS RBC have been identified as most adherent to laminin under flow conditions. We investigated the ability of low-and high-density SS RBC to interact with laminin under various conditions and explored factors that might be responsible for the differences in B-CAM/LU-laminin interaction between high-and low-density SS RBC. We confirmed that high-density SS RBC adhere to laminin more strongly than low-density SS RBC under flow conditions. However, low-density SS RBC bind soluble laminin most strongly and are the most adherent to laminin under static conditions. Soluble recombinant Lutheran extracellular domain protein completely blocked SS RBC adhesion to laminin under both static and flow conditions. The protein kinase A inhibitor 14-22 amide inhibited adhesion to laminin during flow by high-density SS RBC from patients with strongly adherent cells but had no effect on adhesion observed after a static phase. Deletion of the cytoplasmic domain of B-CAM as well as mutation of the juxtamembranous tyrosine residue failed to reduce B-CAM-mediated adhesion to laminin by transfected MEL cells. These studies confirm that B-CAM/LU is the most critical receptor mediating adhesion to laminin under both static and flow conditions. Dense SS RBC are most adherent to laminin despite bearing fewer laminin receptors, apparently due to a reversible protein kinase A-dependent process that is unlikely to involve direct phosphorylation of B-CAM/LU. Our results also suggest that the nature of the interaction of B-CAM/LU with laminin may be different under static and flow conditions. Am.

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Section: Discussionmentioning

confidence: 99%

Section: Evidence That Protein Kinase a Contributes To Increased Hd Smentioning

confidence: 91%

Section: Flow Chamber Assaysmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

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B‐CAM/LU expression and the role of B‐CAM/LU activation in binding of low‐ and high‐density red cells to laminin in sickle cell disease

et al. 2004

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Upregulation of BCAM and its sense lncRNA BAN are associated with gastric cancer metastasis and poor prognosis

et al. 2020

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Patients with metastatic gastric cancer (GC) have a poor prognosis; however, the molecular mechanism of GC metastasis remains unclear. Here, we employed bioinformatics to systematically screen the metastasis‐associated genes and found that the levels of basal cell adhesion molecule (BCAM) were significantly increased in GC tissues from patients with metastasis, as compared to those without metastasis. The upregulation of BCAM was also significantly associated with a shorter survival time. Depletion of BCAM inhibited GC cell migration and invasion. Knockout (KO) of BCAM by the CRISPR/Cas9 system reduced the invasion and metastasis of GC cells. To explore the mechanism of BCAM upregulation, we identified a previously uncharacterized BCAM sense lncRNA that spanned from exon 6 to intron 6 of BCAM, and named it as BCAM‐associated long noncoding RNA (BAN). Knockdown of BAN inhibited BCAM expression at both mRNA and protein levels. Knockdown of BAN suppressed GC cell migration and invasion, which was effectively rescued by ectopic expression of BCAM. Further clinical data showed that BAN upregulation was associated with GC metastasis and poor prognosis. Importantly, BAN expression was also significantly associated with that of BCAM in GC tissues. Taken together, these results indicate that increased expression of BCAM and its sense lncRNA BAN promote GC cell invasion and metastasis, and are associated with poor prognosis of GC patients.

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Functions of Blood Group Antigens

Pawloski¹,

Telen²

2005

Molecular Hematology

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Novel epinephrine and cyclic AMP-mediated activation of BCAM/Lu-dependent sickle (SS) RBC adhesion

Abstract: The vasoocclusive crisis is the major clinical feature of sickle cell anemia, which is believed to be initiated or sustained by sickle (

Cited by 156 publications

References 35 publications

B‐CAM/LU expression and the role of B‐CAM/LU activation in binding of low‐ and high‐density red cells to laminin in sickle cell disease

B‐CAM/LU expression and the role of B‐CAM/LU activation in binding of low‐ and high‐density red cells to laminin in sickle cell disease

Upregulation of BCAM and its sense lncRNA BAN are associated with gastric cancer metastasis and poor prognosis

Functions of Blood Group Antigens

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