Bacterial lipopolysaccharide modulates Protein Kinase C signalling in <i>Lymnaea stagnalis</i> haemocytes

Walker, Anthony J.; Plows, Louise D.

doi:10.1016/j.biolcel.2003.09.001

Cited by 23 publications

(27 citation statements)

References 35 publications

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“…This was unexpected given the involvement of PKC in both PMA-and laminarininduced H 2 O 2 release by L. stagnalis hemocytes [20] as well as in vertebrate cells as described previously [21]. In addition, the importance of PKC in a variety of molluscan immune-related functions has become increasingly apparent in recent years [23,24]. Perhaps the task PKC carries out in PMA-induced H 2 O 2 release is achieved by a different signaling protein(s) such as PI 3 K or PLA 2 in the BSA-gal induced pathway.…”

Section: Discussionmentioning

confidence: 88%

Regulation of hydrogen peroxide release in circulating hemocytes of the planorbid snail Biomphalaria glabrata

Humphries

Yoshino

2008

Developmental & Comparative Immunology

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Biomphalaria spp. serve as obligate intermediate hosts for the human blood fluke Schistosoma mansoni. Following S. mansoni penetration of Biomphalaria glabrata, hemocytes of resistant snails migrate towards the parasite, encasing the larva in a multicellular capsule resulting in its destruction via a cytotoxic reaction. Recent studies have revealed the importance of hydrogen peroxide and nitric oxide (H 2 O 2 , NO) in parasite killing [1,2]. It is assumed H 2 O 2 and NO production is tightly regulated although the specific molecules involved remain largely unknown. Consequently, the potential role of cell signaling pathways in B. glabrata hemocyte H 2 O 2 production was investigated by evaluating the effects of specific inhibitors of selected signaling proteins. Results suggest that both ERK and p38 MAPKs are involved in the regulation of B. glabrata H 2 O 2 release in response to stimulation by PMA and galactose-conjugated BSA. However, the involvement of the signaling proteins PKC, PI 3 kinase and PLA 2 differs between PMA-and BSA-gal-induced H 2 O 2 production.

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Section: Discussionmentioning

confidence: 88%

Regulation of hydrogen peroxide release in circulating hemocytes of the planorbid snail Biomphalaria glabrata

Humphries

Yoshino

2008

Developmental & Comparative Immunology

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“…Bisindolylmaleimide I and H89 were used at concentrations of 4 and 10 μM, respectively. These doses were used in previous cell-based studies to inhibit PKC and PKA activity (59,60).…”

Section: Lc-ms/msmentioning

confidence: 99%

Angiotensin II signaling via protein kinase C phosphorylates Kelch-like 3, preventing WNK4 degradation

Shibata

Arroyo

Castañeda‐Bueno

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

102

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Hypertension contributes to the global burden of cardiovascular disease. Increased dietary K + reduces blood pressure; however, the mechanism has been obscure. Human genetic studies have suggested that the mechanism is an obligatory inverse relationship between renal salt reabsorption and K + secretion. Mutations in the kinases with-no-lysine 4 (WNK4) or WNK1, or in either Cullin 3 (CUL3) or Kelch-like 3 (KLHL3)-components of an E3 ubiquitin ligase complex that targets WNKs for degradation-cause constitutively increased renal salt reabsorption and impaired K + secretion, resulting in hypertension and hyperkalemia. The normal mechanisms that regulate the activity of this ubiquitin ligase and levels of WNKs have been unknown. We posited that missense mutations in KLHL3 that impair binding of WNK4 might represent a phenocopy of the normal physiologic response to volume depletion in which salt reabsorption is maximized. We show that KLHL3 is phosphorylated at serine 433 in the Kelch domain (a site frequently mutated in hypertension with hyperkalemia) by protein kinase C in cultured cells and that this phosphorylation prevents WNK4 binding and degradation. This phosphorylation can be induced by angiotensin II (AII) signaling. Consistent with these in vitro observations, AII administration to mice, even in the absence of volume depletion, induces renal KLHL3 S433 phosphorylation and increased levels of both WNK4 and the NaCl cotransporter. Thus, AII, which is selectively induced in volume depletion, provides the signal that prevents CUL3/KLHL3-mediated degradation of WNK4, directing the kidney to maximize renal salt reabsorption while inhibiting K + secretion in the setting of volume depletion.renin-angiotensin-aldosterone system | distal tubule | hypertension | posttranslational modification | PHAII H ypertension affects 1 billion people worldwide and is a major risk factor for death from stroke, myocardial infarction, and congestive heart failure. The study of Mendelian forms of hypertension has demonstrated the key role of increased renal salt reabsorption in disease pathogenesis (1-4). Observational and intervention trials (5, 6) also indicate that increased dietary K + lowers blood pressure; however, the mechanism of this effect has been unclear.Pseudohypoaldosteronism type II (PHAII; Online Mendelian Inheritance in Man no. 145260), featuring hypertension and hyperkalemia, has revealed a previously unrecognized mechanism that regulates the balance between renal salt reabsorption and K + secretion in response to aldosterone (7). Aldosterone is produced by the adrenal glomerulosa in volume depletion, in response to angiotensin II (AII), and in hyperkalemia via membrane depolarization (8). In volume depletion, aldosterone maximizes renal salt reabsorption, whereas in hyperkalemia, aldosterone promotes maximal renal K + secretion. Volume depletion increases both the NaCl cotransporter (NCC) (9) and electrogenic Na + reabsorption via the epithelial Na + channel (ENaC) (10). The lumen-negative potential produced by ENa...

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“…This antibody has previously been validated for use in L. stagnalis haemocytes (Walker and Plows, 2003) and also has been employed to study PKC phosphorylation in M. galloprovincialis haemocytes (Canesi et al, 2005). When L. stagnalis haemocytes were exposed to 10·mg·ml -1 laminarin, a rapid increase in phosphorylation of an 85·kDa PKC likeprotein was observed, with maximum phosphorylation occurring at 10·min (Fig.·1A, upper panel).…”

Section: Laminarin Stimulates the Phosphorylation Of L Stagnalismentioning

confidence: 99%

“…Discussion Current knowledge of cell signalling in molluscs is poor, and much remains to be discovered concerning the specific signalling molecules that regulate defence reactions, triggered by infection, in this important group of organisms. Using the model snail L. stagnalis, we have recently shown that bacterial LPS modulates the phosphorylation (activation) of PKC (Walker and Plows, 2003) and ERK pathway members (Plows et al, 2004) in haemocytes, cells that play a crucial role in the molluscan defence response. The present research aimed to investigate the effects of laminarin on the activation of PKC like-proteins in L. stagnalis haemocytes and to identify some of the upstream regulators and downstream targets of PKC in these cells.…”

Section: Production Of H 2 O 2 By Laminarin-stimulated Haemocytes Ismentioning

confidence: 99%

“…In this context, the ERK 1/2 pathway has been characterized in an embryonic cell line from the gastropod snail Biomphalaria glabrata (Humphries et al, 2001) and in L. stagnalis (Plows et al, 2004). Work in our laboratory has led to the detection of PKC-like proteins in L. stagnalis haemocytes and has shown that PKC phosphorylation and activation are modulated following LPS challenge (Walker and Plows, 2003). Further research also showed that PKC and ERK play a role in phagocytosis (Plows et al, 2004) and the production of nitric oxide (NO) (Wright et al, 2006) by L. stagnalis haemocytes.…”

Section: Introductionmentioning

confidence: 99%

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β-1, 3-glucan modulates PKC signalling inLymnaea stagnalisdefence cells: a role for PKC in H2O2 production and downstream ERK activation

Lacchini

Davies

Mackintosh

et al. 2006

Journal of Experimental Biology

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SUMMARY Haemocytes from the gastropod snail Lymnaea stagnalis (Linnaeus)were used as a model to characterize protein kinase C (PKC) signalling events in molluscan defence cells. Challenge of freshly collected haemocytes with theβ-1, 3-glucan laminarin resulted in a transient increase in the phosphorylation of haemocyte PKC, with maximal phosphorylation (represented by a 3.5-fold increase) occurring at 10 min; this effect was blocked by the PKC inhibitor, GF109203X. Moreover, extracellular signal-regulated kinase (ERK)was found to be a downstream target of molluscan PKC, operating via a MAPK/ERK kinase (MEK)-dependent mechanism. Pharmacological inhibition of PKC phosphorylation by U-73122 and ET-18-OCH3 suggested that laminarin-dependent PKC signalling was modulated via phospholipase C(PLC); however, a role for phosphatidylinositol-3-kinase (PI-3-K) is unlikely since the PI-3-K inhibitor LY294002 was without effect. Generation of H2O2 by haemocytes in response to laminarin was also investigated. H2O2 output increased in a dose- and time-dependent manner, with 10 mg ml-1 laminarin eliciting a 9.5-fold increase in H2O2 production after 30 min. H2O2 production was significantly attenuated by the PKC inhibitors, GF109203X and Gö 6976, and by the NADPH-oxidase inhibitor,apocynin. In conclusion, these data further our understanding of PKC signalling events in molluscan haemocytes and for the first time define a role for PKC in H2O2 production by these defence cells. Given that H2O2 is an important anti-pathogen molecule, and that haemocytes play a crucial role in the elimination of invading organisms,PKC signalling in these cells is likely to be crucial to the molluscan innate defence response.

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Bacterial lipopolysaccharide modulates Protein Kinase C signalling in Lymnaea stagnalis haemocytes

Cited by 23 publications

References 35 publications

Regulation of hydrogen peroxide release in circulating hemocytes of the planorbid snail Biomphalaria glabrata

Regulation of hydrogen peroxide release in circulating hemocytes of the planorbid snail Biomphalaria glabrata

Angiotensin II signaling via protein kinase C phosphorylates Kelch-like 3, preventing WNK4 degradation

β-1, 3-glucan modulates PKC signalling inLymnaea stagnalisdefence cells: a role for PKC in H2O2 production and downstream ERK activation

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