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Enregistrement W4389243607 · doi:10.1182/blood-2023-179047

The Role of Gpibα in Control of Megakaryocyte Reactivity to Thrombopoietin

2023· article· en· W4389243607 sur OpenAlexaff
Fengjiao Han, Qiuyu Guo, Yun Wang, Zihan Zhang, Qi Feng, Jun Peng, Ming Hou, Heyu Ni, Miao Xu

Notice bibliographique

RevueBlood · 2023
Typearticle
Langueen
DomaineMedicine
ThématiquePlatelet Disorders and Treatments
Établissements canadiensUniversity of Toronto
Organismes subventionnairesnon disponible
Mots-clésThrombopoietinMegakaryocytePlateletThrombopoiesisHaematopoiesisInternal medicineEndocrinologyBone marrowChemistryImmunologyWild typeBiologyCell biologyMedicineStem cellMutantBiochemistry

Résumé

récupéré en direct d'OpenAlex

Thrombopoietin (TPO) was first described in 1958 as a humoral factor that regulates platelet production. TPO binds to c-Mpl and stimulates the expansion and differentiation of megakaryocyte precursors and the maturation of megakaryocytes. Notably, TPO has no significant effect on the formation stage of megakaryocyte boundary membrane system and platelet release. Studies investigating GPIbα deficiency have demonstrated its substantial effects on megakaryocyte proliferation, ploidy maturation, and resultant platelet count reduction. Furthermore, our previous study demonstrated that GPIbα deficiency in mice and patients with Bernard-Soulier syndrome (BSS) results in reduced circulating TPO levels. Surprisingly, this decrease in TPO levels is not due to increased TPO clearance by platelets lacking GPIbα but rather a decrease in TPO production, which is regulated by GPIbα through the interaction with liver cells. Based on these findings, we hypothesize that augmenting exogenous TPO levels may effectively promote platelet production in GPIbα deficiency. We first generated C57/BL6 background GPIbα deficiency mice and measured their platelet levels using an automatic blood routine counter, confirming previous findings of a lower platelet count in GPIbα deficiency mice. Subsequently, both GPIbα deficiency and wild-type mice were intraperitoneally injected with recombinant mouse TPO (rmTPO) simultaneously. Surprisingly, we observed that the GPIbα deficiency mice exhibited reduced reactivity to TPO, resulting in a significant decrease in platelet production compared to wild-type mice. To elucidate it mechanism, we conducted comprehensive studies in vitro, isolating bone marrow-derived lin- cells from both GPIbα-deficient and wild-type mice using magnetic beads. These cells were then cultured in the presence of rmTPO, and the results revealed that GPIbα deficiency led to the inhibition of megakaryocyte cell ploidy maturation and platelet production compared to wild-type mice. Furthermore, we designed RNA small interference sequences targeting GPIbα. By conducting in vitro interference experiment using wild-type mice bone marrow-derived lin- cells with TPO, the knockdown of GPIbα resulted in inhibited megakaryocyte cell ploidy maturation and platelet production, consistent with the findings from the deficiency mice. In addition to our prior experiments investigating the GPIbα mediated TPO generation, we have also explored the impact of GPIbα antibodies on TPO production, revealing a significant reduction in TPO levels among GPIbα-positive immune thrombocytopenia (ITP) patients. These data raise our curiosity regarding the responsiveness to TPO in ITP, particularly among GPIbα-positive ITP patients. To verify our hypothesis, a retrospective analysis was performed to assess the response to TPO-related treatments in ITP patients, including eltrombopag, romiplostim, avatrombopag and recombinant human thrombopoietin (rhTPO). The outcomes observed in ITP patients positive for GPIbα antibodies revealed noteworthy patterns. The retrospective analysis revealed that ITP patients exhibiting GPIbα positivity displayed a worse response to thrombopoietin receptor agonists (TPO-RA) and rhTPO treatment. To gain deeper insights into the aforementioned findings, we conducted in vitro investigations on antibody-bound megakaryocytes. Specifically, we cultured wild-type mice bone marrow-derived lin- cells in the presence of TPO, with or without anti-GPIbα antibody intervention. The antibody group exhibited inhibition of megakaryocyte ploidy maturation and platelet production compared to the negative control group. In summary, our findings suggest that GPIbα plays a critical role in control of TPO reactivity, and its absence or interference can lead to impaired megakaryocyte ploidy maturation and platelet production. Moreover, ITP patients with anti-GPIbα antibody is associated with decreased TPO responsiveness, probably contributing to the observed poor response to TPO-based treatments. These findings have significant clinical implications, shedding light on platelet-related disorders and potential therapeutic strategies. Specifically, understanding the influence of GPIbα on megakaryocyte TPO reactivity will offer avenues for novel therapeutic interventions targeting platelet-related disorders.

Récupéré en direct depuis OpenAlex et désinversé. Les résumés ne sont pas conservés dans cette base de données : les index inversés représentent 8,6 Go des 9,3 Go de texte de la base, et le serveur dispose de 13 Go libres.

Comment cette classification a été obtenuedéplier

Prédiction machine sur la base complète

Imitation des enseignants

Ni prévalence calibrée, ni vérité terrain. Validation humaine à venir. Le volet Gemma est une étiquette directe du modèle pour chaque travail de la base, lue sur la notice réduite au titre. Le volet Codex est un classifieur appris des 10 348 étiquettes directes de Codex et calibré sur les taux pondérés de l'échantillon; les champs sans appui suffisant ne portent aucun appel Codex. Le mode candidate est l'union des deux volets; le consensus est leur intersection. Ces sorties portent le statut machine_predicted_unvalidated et ne sont pas des étiquettes humaines.

score de la tête « metaresearch » (Codex)0,000
score de la tête « metaresearch » (Gemma)0,000
Version: metacan-v3-hybrid-931329e0061cStatut de validation: machine_predicted_unvalidated
Catégories candidatesaucune
Catégories consensuellesaucune
DomaineSignal candidat: aucune · Signal consensuel: aucune
Devis d'étudeSignal candidat: Expérimental (laboratoire) · Signal consensuel: Expérimental (laboratoire)
GenreSignal candidat: Empirique · Signal consensuel: Empirique
Score de désaccord entre enseignants0,000
Score d'incertitude au seuil0,002

Scores du classifieur distillé par catégorie (deux têtes)

CatégorieCodexGemma
Métarecherche0,0000,000
Méta-épidémiologie (sens strict)0,0000,000
Méta-épidémiologie (sens large)0,0000,000
Bibliométrie0,0000,000
Études des sciences et des technologies0,0000,000
Communication savante0,0000,000
Science ouverte0,0000,000
Intégrité de la recherche0,0000,000
Charge utile insuffisante (le modèle a refusé de juger)0,0000,000

Scores machine (provisoires)

Les deux têtes enseignantes du modèle étudiant, lues sur ce travail. Un score ordonne la base pour la relecture; il n'affirme jamais une catégorie, et le statut de validation accompagne chaque rangée tel quel.

Scores de référence d'un modèle non mature (critères de maturité non atteints, 7 itérations). Un score ordonne; il n'affirme jamais une catégorie.

Tête enseignante Opus0,008
Tête enseignante GPT0,251
Écart entre enseignants0,243 · la distance entre les deux têtes enseignantes sur ce seul travail
Statut de validationscore_only:v0-immature-baseline · tel quel depuis la passe de notation : score_only signifie que le nombre peut ordonner les travaux, et qu'aucune étiquette de catégorie n'en découle

Classification

machine, non validée

Prédiction automatique; un appel candidat d’une seule source (Gemma direct ou Codex distillé), pas un consensus.

Les modèles n’ont appliqué aucune catégorie : rien dans la taxonomie ne correspondait à ce travail.
Devis d'étudeExpérimental (laboratoire)
Domainenon disponible
GenreEmpirique

Le détail, modèle par modèle et score par score, se trouve en fin de page sous « Comment cette classification a été obtenue ».

En bref

Citations0
Publié2023
Routes d'admission1
Résumé présentoui

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