Platelet Density and Size in Inflammatory Bowel Disease

Järemo, Petter; Sandberg-Gertzén, Hanna

doi:10.1055/s-0038-1650321

Cited by 76 publications

(63 citation statements)

References 5 publications

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“…35 Multiple platelet abnormalities have been identified in patients with IBD, including reactive thrombocytosis, low mean platelet volume, and increased density. [47][48][49] Importantly, platelets in IBD patients circulate in the periphery in an increased activated state and are more susceptible to activation than platelets from healthy participants. 50 Here, we present yet another abnormality associated with platelets from patients with IBD.…”

Section: Discussionmentioning

confidence: 99%

Platelet hyaluronidase-2: an enzyme that translocates to the surface upon activation to function in extracellular matrix degradation

Albeiroti

Ayasoufi

Hill

et al. 2015

Blood

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• Platelet HYAL2 is stored in a-granules and upon activation it becomes surface expressed where it functions to degrade extracellular matrix.• Platelets from IBD patients contain lower HYAL2 protein and activity than those from non-IBD controls.Following injury, platelets rapidly interact with the exposed extracellular matrix (ECM) of the vessel wall and the surrounding tissues. Hyaluronan (HA) is a major glycosaminoglycan component of the ECM and plays a significant role in regulating inflammation. We have recently reported that human platelets degrade HA from the surfaces of activated endothelial cells into fragments capable of inducing immune responses by monocytes. We also showed that human platelets contain the enzyme hyaluronidase-2 (HYAL2), one of two major hyaluronidases that digest HA in somatic tissues. The deposition of HA increases in inflamed tissues in several inflammatory diseases, including inflammatory bowel disease (IBD). We therefore wanted to define the mechanism by which platelets degrade HA in the inflamed tissues. In this study, we show that human platelets degrade the proinflammatory matrix HA through the activity of HYAL2 and that platelet activation causes the immediate translocation of HYAL2 from a distinct population of a-granules to platelet surfaces where it exerts its catalytic activity. Finally, we show that patients with IBD have lower platelet HYAL2 levels and activity than healthy controls. (Blood. 2015; 125(9):1460-1469 Introduction Hyaluronan (HA) is a ubiquitous glycosaminoglycan and a major component of the extracellular matrix (ECM), and it has a crucial role in regulating inflammation.1 HA is produced by the HA synthase enzymes (HAS1-3) and is composed of repeating disaccharides of D-glucuronic acid and N-acetylglucosamine. Not only can HA be synthesized and released, but it can also form a voluminous pericellular coat that surrounds cells. The HA coat is either anchored to the cell surface through binding to specific cell-surface receptors, such as CD44, or it can be retained at the cell surface by sustained transmembrane interactions with its synthases.2 Interestingly, a growing body of literature suggests that different sizes of HA exert a wide spectrum of functions.3 Under normal conditions in tissues, HA is present in its high molecular weight (HMWHA) form (1 to 10 3 10 6 Da). HMWHA functions as a structural hydrating polymer and is also known to be antiinflammatory, 4 protecting from T-cellmediated liver injury and bleomycin-mediated lung injury in mice. 5,6 HMWHA also promotes the suppressive effects of regulatory CD4 1 CD251 T cells. 7Increased HA deposition has also been reported in many inflammatory diseases including inflammatory bowel disease (IBD), arthritis, and asthma. [8][9][10] Importantly, degradation of HA results in HA fragments that function as damage-associated molecular patterns. 11Fragmented HA contributes to wound healing, angiogenesis, and inflammation and is capable of signaling cellular responses through specific receptors. 12 For example, HA ...

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Section: Discussionmentioning

confidence: 99%

Platelet hyaluronidase-2: an enzyme that translocates to the surface upon activation to function in extracellular matrix degradation

Albeiroti

Ayasoufi

Hill

et al. 2015

Blood

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“…There are many studies performed on adults that indicate that MPV values may be a valuable method in the diagnosis of acute appendicitis [13]. It is proposed that in acute inflammatory conditions activated leucocytes secrete interleukin-6 that causes a decrease in MPV value by reducing platelet production [12,[20][21][22]24]. In the literature, MPV has been reported to decrease in some inflammatory bowel diseases such as ulcerative colitis, especially in the active period, and that it could be used for determination of the disease activity .…”

Section: Discussionmentioning

confidence: 99%

“…In the literature, MPV has been reported to decrease in some inflammatory bowel diseases such as ulcerative colitis, especially in the active period, and that it could be used for determination of the disease activity . [12,15,[23][24][25] The pathogenesis of this decrease in MPV has not been fully explained, it seems reasonable to explain this with the consumption and sequestration of large active platelets in the vascular segments of the inflamed bowel as Danese et al claimed [26].…”

Section: Discussionmentioning

confidence: 99%

Role of Mean Platelet Volume (MPV) In Diagnosis of Acute Appendicitis

Saxena¹,

Tandon²,

Gedam³

2015

Int Jour of Biomed Res

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The diagnosis of acute appendicitis still remains an enigma for the surgeon. The Mean Platelet volume is known to be a marker determined from megakaryocytes during platelet production, which is associated with platelet function and activation. The mean platelet volume (MPV) decreases in acute inflammatory conditions like acute appendicitis due to increased consumption and sequestration of platelets in the vascular segments of inflamed bowel. In our study of 213 patients, the MPV was determined and was found to be low (< 7.6fL) in 176 patients (82.6%) out of which 175 patients were having features of acute appendicitis on histopathology. Therefore in a patient with a provisional diagnosis of acute appendicitis, a low MPV (<7.6fL) can be taken into consideration along with total leucocyte count with suspected acute appendicitis.

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“…In many studies it was documented that platelets increase systemic inflammatory response by secreting inflammatory mediators in IBD (18)(19)(20)(21)(22)(23)(24). While it is observed platelet number in IBD is affected, it is shown MPV decreases (25)(26)(27). Contrary to this, MPV increase in peripheral blood has direct proportion to platelet function (28).…”

Section: Introductionmentioning

confidence: 99%