scholarly journals Mechanism of kinetin-induced death of Vicia faba ssp. minor root cortex cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Andrzej Kaźmierczak ◽  
Anita Kunikowska ◽  
Magdalena Doniak ◽  
Andrzej Kornaś
Keyword(s):  
Cell Death ◽  
Vicia Faba ◽  
Permeability Transition ◽  
Ruthenium Red ◽  
Root Cortex ◽  
Raf Kinase ◽  
Cytokinin Receptors ◽  
Root Cortex Cells ◽  
Exogenous Factors

AbstractCell death (CD) may be induced by endogenous or exogenous factors and contributes to all the steps of plant development. This paper presents results related to the mechanism of CD regulation induced by kinetin (Kin) in the root cortex of Vicia faba ssp. minor. To explain the process, 6-(2-hydroxy-3-methylbenzylamino)purine (PI-55), adenine (Ad), 5′-amine-5′-deoxyadenosine (Ado) and N-(2-chloro-4-piridylo)-N′-phenylurea (CPPU) were applied to (i) block cytokinin receptors (CKs) and inhibit the activities of enzymes of CK metabolism, i.e., (ii) phosphoribosyltransferase, (iii) kinases, and (iv) oxidases, respectively. Moreover, ethylene glycol-bis(β-aminoethyl ether)-N,N,N′,N′-tetraacetic acid (EGTA), lanthanum chloride (LaCl3), ruthenium red (RRed) and cyclosporine A (CS-A) were applied to (i) chelate extracellular calcium ions (Ca2+) as well as blocks of (ii) plasma-, (iii) endoplasmic reticulum- (ER) membrane Ca2+ ion channels and (iv) mitochondria- (MIT) Ca2+ ions release by permeability transition por (PTP), respectively. The measured physiological effectiveness of these factors was the number of living and dying cortex cells estimated with orange acridine (OA) and ethidium bromide (EB), the amounts of cytosolic Ca2+ ions with chlortetracycline (CTC) staining and the intensity of chromatin and Ca2+-CTC complex fluorescence, respectively. Moreover, the role of sorafenib, an inhibitor of RAF kinase, on the vitality of cortex cells and ethylene levels as well as the activities of RAF-like kinase and MEK2 with Syntide-2 and Mek2 as substrates were studied. The results clarified the previously presented suggestion that Kin is converted to appropriate ribotides (5′-monophosphate ribonucleotides), which cooperate with the ethylene and Ca2+ ion signalling pathways to transduce the signal of kinetin-programmed cell death (Kin-PCD). Based on the present and previously published results related to Kin-PCD, the crosstalk between ethylene and MAP kinase signalling, as well as inhibitors of CK receptors and enzymes of their metabolism, is proposed.

scholarly journals Mechanism of kinetin-induced death of Vicia faba ssp. minor cortex cells

2021 ◽  
Author(s):  
Andrzej Kaźmierczak ◽  
Anita Kunikowska ◽  
Magdalena Doniak ◽  
Andrzej Kornaś
Keyword(s):  
Vicia Faba ◽  
Calcium Ions ◽  
Calcium Ion ◽  
Map Kinases ◽  
Tetraacetic Acid ◽  
Ethylene Signaling ◽  
Root Cortex ◽  
Raf Kinase ◽  
Exogenous Factors

Abstract Cell death (CD) takes part in the control of all the steps of plant development. It may be induced by endogenous or exogenous factors. This paper presents the results related to mechanism of CD regulation induced by kinetin (Kin) in root cortex of Vicia faba ssp. minor. To explain the process 6-(2-hydroxy-3-methylbenzylamino)purine (PI-55), adenine (Ad), 5'-amine-5'-deoxyadenosine (Ado) and N-(2-chloro-4-piridylo)-N’-phenylurea (CPPU) were applied to (i) block cytokinins (CKs) receptors and toinhibit the activity of (ii) kinases, (iii) oxidases and (iv) phosphoribosyltransferase, respectively. Moreover, ethylene glycol-bis(β-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), lanthanum chloride (LaCl3) and cyclosporine (CsA) were applied to inactivate calcium ion (Ca2+) channels (i) across all membranes (ALM-Ca2+), including (ii) endoplasmic reticulum (ER-Ca2+) and (iii) mitochondria (MIT-Ca2+), respectively. The effects of these factors were measured by estimation of vitality of cortex cells and amounts of cytosolic Ca2+. Additionally, the role of Sorafenib, inhibitor of RAF kinase, on vitality of cortex cells and ethylene amount as well as the activities of Raf-like kinase and MEK2 with Syntide and Mek2 as substrates, were studied. The results of the paper clarified the suggestion that Kin was converted directly or indirectly to appropriate ribotides (5’-monophosphate ribonucleotides) which cooperated with ethylene and calcium ions signaling pathway activating CD by Kin (Kin-ECD) exogenously (E). Based on the present and previously published results, the scheme of the crosstalk between ethylene signaling MAP kinases, CKs receptor and enzymes of their metabolism in induction of Kin-ECD is proposed.

scholarly journals Kinetin induces cell death in root cortex cells of Vicia faba ssp. minor seedlings

PROTOPLASMA ◽  
2012 ◽  
Vol 250 (4) ◽  
pp. 851-861 ◽  
Author(s):  
Anita Kunikowska ◽  
Anna Byczkowska ◽  
Andrzej Kaźmierczak
Keyword(s):  
Cell Death ◽  
Vicia Faba ◽  
Root Cortex ◽  
Root Cortex Cells

scholarly journals JNK1/2 regulates ER–mitochondrial Ca2+ cross-talk during IL-1β–mediated cell death in RINm5F and human primary β-cells

2013 ◽  
Vol 24 (12) ◽  
pp. 2058-2071 ◽  
Author(s):  
Gaurav Verma ◽  
Himanshi Bhatia ◽  
Malabika Datta
Keyword(s):  
Cell Death ◽  
Er Stress ◽  
Mitochondrial Permeability Transition ◽  
Apoptotic Cell ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Β Cells ◽  
Mediating Role ◽  
Induced Apoptosis

Elevated interleukin-1β (IL-1β) induces apoptosis in pancreatic β-cells through endoplasmic reticulum (ER) stress induction and subsequent c-jun-N-terminal kinase 1/2 (JNK1/2) activation. In earlier work we showed that JNK1/2 activation is initiated before ER stress and apoptotic induction in response to IL-1β. However, the detailed regulatory mechanisms are not completely understood. Because the ER is the organelle responsible for Ca2+ handling and storage, here we examine the effects of IL-1β on cellular Ca2+ movement and mitochondrial dysfunction and evaluate the role of JNK1/2. Our results show that in RINm5F cells and human primary β-cells, IL-1β alters mitochondrial membrane potential, mitochondrial permeability transition pore opening, ATP content, and reactive oxygen species production and these alterations are preceded by ER Ca2+ release via IP3R channels and mitochondrial Ca2+ uptake. All these events are prevented by JNK1/2 small interfering RNA (siRNA), indicating the mediating role of JNK1/2 in IL-1β–induced cellular alteration. This is accompanied by IL-1β–induced apoptosis, which is prevented by JNK1/2 siRNA and the IP3R inhibitor xestospongin C. This suggests a regulatory role of JNK1/2 in modulating the ER-mitochondrial-Ca2+ axis by IL-1β in apoptotic cell death.

Role of Calcium Homeostasis in Ischemic Stroke: A Review

2021 ◽  
Vol 20 ◽  
Author(s):  
Abhilash Ludhiadch ◽  
Rashmi Sharma ◽  
Aishwarya Muriki ◽  
Anjana Munshi
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Neuronal Death ◽  
Complex Disease ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition ◽  
Vital Role ◽  
Calcium Accumulation ◽  
Cell Death Pathway

: Stroke is the second most common cause of death worldwide. It occurs due to the insufficient supply of oxygen-rich blood to the brain. It is a complex disease with multiple associated risk factors including smoking, alcoholism, age, sex, ethnicity, etc. Calcium ions are known to play a vital role in cell death pathways, which is a ubiquitous intracellular messenger during and immediately after an ischemic period. Disruption in normal calcium hemostasis is known to be a major initiator and activator of the ischemic cell death pathway. Under Ischemic stroke conditions, glutamate is released from the neurons and glia which further activates the N-methyl-D-aspartate (NMDA) receptor and triggers the rapid translocation of Ca2+ from extracellular to intracellular spaces in cerebral tissues and vice versa. Various studies indicated that Ca2+ could have harmful effects on neurons under acute ischemic conditions. Mitochondrial dysfunction also contributes to delayed neuronal death, and it was established decades ago that massive calcium accumulation triggers mitochondrial damage. Elevated Ca2+ levels cause mitochondria to swell and release their contents. As a result oxidative stress and mitochondrial calcium accumulation activate mitochondrial permeability transition and lead to depolarization-coupled production of reactive oxygen species. This association between calcium levels and mitochondrial death suggests that elevated calcium levels might have a role in the neurological outcome in ischemic stroke. Previous studies have also reported that elevated Ca2+ levels play a role in the determination of infarct size, outcome, and recurrence of ischemic stroke. The current review has been compiled to understand the multidimensional role of altered Ca2+ levels in the initiation and alteration of neuronal death after ischemic attack. The underlying mechanisms understood to date have also been discussed.

scholarly journals HAX-1 regulates cyclophilin-D levels and mitochondria permeability transition pore in the heart

2015 ◽  
Vol 112 (47) ◽  
pp. E6466-E6475 ◽  
Author(s):  
Chi Keung Lam ◽  
Wen Zhao ◽  
Guan-Sheng Liu ◽  
Wen-Feng Cai ◽  
George Gardner ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Mitochondrial Membrane ◽  
Human Lymphocytes ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Cyclophilin D ◽  
Membrane Function ◽  
Genetic Ablation

The major underpinning of massive cell death associated with myocardial infarction involves opening of the mitochondrial permeability transition pore (mPTP), resulting in disruption of mitochondria membrane integrity and programmed necrosis. Studies in human lymphocytes suggested that the hematopoietic-substrate-1 associated protein X-1 (HAX-1) is linked to regulation of mitochondrial membrane function, but its role in controlling mPTP activity remains obscure. Herein we used models with altered HAX-1 expression levels in the heart and uncovered an unexpected role of HAX-1 in regulation of mPTP and cardiomyocyte survival. Cardiac-specific HAX-1 overexpression was associated with resistance against loss of mitochondrial membrane potential, induced by oxidative stress, whereas HAX-1 heterozygous deficiency exacerbated vulnerability. The protective effects of HAX-1 were attributed to specific down-regulation of cyclophilin-D levels leading to reduction in mPTP activation. Accordingly, cyclophilin-D and mPTP were increased in heterozygous hearts, but genetic ablation of cyclophilin-D in these hearts significantly alleviated their susceptibility to ischemia/reperfusion injury. Mechanistically, alterations in cyclophilin-D levels by HAX-1 were contributed by the ubiquitin-proteosomal degradation pathway. HAX-1 overexpression enhanced cyclophilin-D ubiquitination, whereas proteosomal inhibition restored cyclophilin-D levels. The regulatory effects of HAX-1 were mediated through interference of cyclophilin-D binding to heat shock protein-90 (Hsp90) in mitochondria, rendering it susceptible to degradation. Accordingly, enhanced Hsp90 expression in HAX-1 overexpressing cardiomyocytes increased cyclophilin-D levels, as well as mPTP activation upon oxidative stress. Taken together, our findings reveal the role of HAX-1 in regulating cyclophilin-D levels via an Hsp90-dependent mechanism, resulting in protection against activation of mPTP and subsequent cell death responses.

Sign in / Sign up

Export Citation Format

Share Document